There is a new ray of hope for the one million people who suffer from Parkinson's disease. At the University of Iowa, distinguished professor of biomedical sciences Anumantha Kanthasamy has been working for more than ten years to gain a deeper understanding of Parkinson's disease and its
causes. Now, Dr. Kanthasamy has discovered a protein which could be an important key in the search for a treatment and cure for this debilitating disease.
The protein, called kinase-C, targets the dopamine-producing cells in the brain, killing them and causing a drop in dopamine levels. Low dopamine levels are one of the causes of Parkinson's disease. Dr. Kanthasamy states, "We have millions of cells in our brains. In Parkinson's, about 10,000 of these brain cells die; no one knows why." Dopamine is the link in the communication system between our brains and our muscles. Without dopamine, nerves function improperly and the communication breaks down causing a loss in our ability to control our body's movements.
The level of dopamine in our brains drops gradually as we age. In fact, Dr. Kanthasamy states that "everybody has a little Parkinson's in theory." In any older adult, dopamine levels that drop below 60-70 percent will create some Parkinson's-like symptoms. In adults diagnosed with Parkinson's, the dopamine levels continue to drop well below 40 percent causing a marked increase in symptoms such as shakiness, stiffness, fidgeting and jerking.
Kanthasamy states that a patient suffering from Parkinson's could be a "functioning, normal person," if their dopamine levels could be raised back to the 40-50 percent level. They would not need to bring their dopamine levels back to 100 percent. Currently there is no cure for Parkinson's disease, only therapies and medications to treat the symptoms.
For more information go to www.parkinsonresearchfoundation.org
Sunday, December 27, 2009
Sunday, December 13, 2009
Parkinson’s Disease Patients Treated with Autologous Bone Marrow Stem Cells May Improve Their Quality of Life
Eight Parkinson’s Disease patients were treated with their own bone marrow stem cells (BMSC) injected via minimally invasive non-surgical routes and discharged the next morning without complications.
“We show the clinical use of autologous BMSC in PD patients, not in animal tests” leader investigator Dr. Luis Geffner said.
Evaluations with UPDRS, Hoehn & Yahr scale and Schwab & England score showed encouraging improvements such as the graphologic tests performed before and after the trasplant that demonstrated significant differences.
Additionally the total L-dopamine dose could be decreased suggesting that stem cells may enhance endogenous dopamine synthesis. He also explained that they are very cautious and prudent emphasizing that they are not talking about cure but stem cells may possibly be a new tool to complement current treatments and delay the progress either of the illness or its complications such as the side effects of some medication.
This study showing safety and feasibility of autologous adult BMSC transplant in PD patients was presented in Baltimore on October 11th 2009 in the 23rd Annual Symposium of Etiology, Pathogenesis and Treatment of Parkinson’s Disease and other Movement Disorders organized by the Parkinson Study Group in affiliation with the American Neurological Association and published in September 2009 issue of Movement Disorders, a peer -review journal.
Geffner's team has already transplanted 144 patients suffering from different illnesses or trauma states and many of them have been followed up 5 years showing that autologous adult BMSC neither provoke tumors, immunologic rejection, infections nor arise ethical or religious controversies.
Dr. Geffner has been working in the field of clinical application of stem cells since 2001 and is author and co-author of several papers, lecturer in many meetings and has also founded the stem cells research in Ecuador in July 2004.
He is in charge of the Clinical Research & Regenerative Medicine Department of the University Hospital SHDUG of the state University of Guayaquil, Ecuador (www.stemcellsecuador.com).
Programs in various diseases and trauma states are currently being performed by his team and they expect to have new data to publish in the near future.
For more information go to www.parkinsonresearchfoundation.org
“We show the clinical use of autologous BMSC in PD patients, not in animal tests” leader investigator Dr. Luis Geffner said.
Evaluations with UPDRS, Hoehn & Yahr scale and Schwab & England score showed encouraging improvements such as the graphologic tests performed before and after the trasplant that demonstrated significant differences.
Additionally the total L-dopamine dose could be decreased suggesting that stem cells may enhance endogenous dopamine synthesis. He also explained that they are very cautious and prudent emphasizing that they are not talking about cure but stem cells may possibly be a new tool to complement current treatments and delay the progress either of the illness or its complications such as the side effects of some medication.
This study showing safety and feasibility of autologous adult BMSC transplant in PD patients was presented in Baltimore on October 11th 2009 in the 23rd Annual Symposium of Etiology, Pathogenesis and Treatment of Parkinson’s Disease and other Movement Disorders organized by the Parkinson Study Group in affiliation with the American Neurological Association and published in September 2009 issue of Movement Disorders, a peer -review journal.
Geffner's team has already transplanted 144 patients suffering from different illnesses or trauma states and many of them have been followed up 5 years showing that autologous adult BMSC neither provoke tumors, immunologic rejection, infections nor arise ethical or religious controversies.
Dr. Geffner has been working in the field of clinical application of stem cells since 2001 and is author and co-author of several papers, lecturer in many meetings and has also founded the stem cells research in Ecuador in July 2004.
He is in charge of the Clinical Research & Regenerative Medicine Department of the University Hospital SHDUG of the state University of Guayaquil, Ecuador (www.stemcellsecuador.com).
Programs in various diseases and trauma states are currently being performed by his team and they expect to have new data to publish in the near future.
For more information go to www.parkinsonresearchfoundation.org
Thursday, December 3, 2009
Ghrelin hormone "can boost resistance" to Parkinson's
Ghrelin can boost a person's resistance to Parkinson's disease, it has been discovered.
The importance of dopamine in regards to Parkinson's disease has been addressed by researchers in the US.
It is a widely-held understanding that the degeneration of dopamine neurons in an area of the brain known as the substantia nigra - which is responsible for dopamine production - leads to a worsening of conditions.
This can lead to an increased difficulty in walking, restricted movements, a lack of appetite, periods of motionlessness and notable head and limb tremors, according to scientists on the project at the Yale School of Medicine.
Tamas Horvath, the chair of the facility and professor of comparative medicine, explained that he and his team discovered that ghrelin is responsible for directly activating the brain's dopamine calls.
He continued: "Because this hormone originates from the stomach, it is circulating normally in the body, so it could easily be used to boost resistance to Parkinson's or it could be used to slow the development of the disease."
Earlier this month, it was discovered that red tomatoes contain a lot of ghrelin, as well as making a person feel fuller quicker.
For more information go to www.parkinsonresearchfoundation.org
The importance of dopamine in regards to Parkinson's disease has been addressed by researchers in the US.
It is a widely-held understanding that the degeneration of dopamine neurons in an area of the brain known as the substantia nigra - which is responsible for dopamine production - leads to a worsening of conditions.
This can lead to an increased difficulty in walking, restricted movements, a lack of appetite, periods of motionlessness and notable head and limb tremors, according to scientists on the project at the Yale School of Medicine.
Tamas Horvath, the chair of the facility and professor of comparative medicine, explained that he and his team discovered that ghrelin is responsible for directly activating the brain's dopamine calls.
He continued: "Because this hormone originates from the stomach, it is circulating normally in the body, so it could easily be used to boost resistance to Parkinson's or it could be used to slow the development of the disease."
Earlier this month, it was discovered that red tomatoes contain a lot of ghrelin, as well as making a person feel fuller quicker.
For more information go to www.parkinsonresearchfoundation.org
Monday, November 23, 2009
Parkinson's breakthrough brings treatment hope
Australian scientists researching the causes of Parkinson's disease say their breakthrough will help develop new ways of treating other debilitating illnesses.
Neuroscientists at the Garvan Institute in Sydney have discovered how the brain's dopamine nerve cells regulate the release of the hormone to control the body's movements.
The debilitating shaking symptoms of Parkinson's happen when the brain does not produce enough of the substance.
Dr Bryce Vissel says it is a big step forward in treating the disease.
"We're going to be using this method to actually discover how drugs treat Parkinson's disease currently and to make new therapeutic developments that may be completely novel, completely new ways of treating Parkinson's," he said.
Dr James Daniel says the discovery will help develop new drugs to treat the rising number of sufferers, but it also has wider implications.
"We're talking a lot about Parkinson's disease because that's been the primary focus of our research but these cells are also very important in a number of other neurological disorders," he said.
"They're critically implicated in schizophrenia - the model system can be applied exactly the same way to studying that."
For more information go to www.parkinsonresearchfoundation.org
Neuroscientists at the Garvan Institute in Sydney have discovered how the brain's dopamine nerve cells regulate the release of the hormone to control the body's movements.
The debilitating shaking symptoms of Parkinson's happen when the brain does not produce enough of the substance.
Dr Bryce Vissel says it is a big step forward in treating the disease.
"We're going to be using this method to actually discover how drugs treat Parkinson's disease currently and to make new therapeutic developments that may be completely novel, completely new ways of treating Parkinson's," he said.
Dr James Daniel says the discovery will help develop new drugs to treat the rising number of sufferers, but it also has wider implications.
"We're talking a lot about Parkinson's disease because that's been the primary focus of our research but these cells are also very important in a number of other neurological disorders," he said.
"They're critically implicated in schizophrenia - the model system can be applied exactly the same way to studying that."
For more information go to www.parkinsonresearchfoundation.org
Friday, November 13, 2009
Brain Imaging of Early Stage Parkinson’s
By Rick Nauert PhD
A research team from the University of Illinois at Chicago plans to use cutting-edge technology to study early-stage Parkinson’s disease.
They hope that tests using functional and high-resolution structural brain imaging will reveal new clues about early Parkinson’s disease.
Parkinson’s disease is a progressive, debilitating movement disorder pharmaceutically managed by using drugs that compensate for a lack of the neurotransmitter dopamine. Parkinson’s patients have a deficit of this important chemical because of degeneration in an area of the brain stem where it is made — a structure called the substantia nigra.
The National Institutes of Health has awarded David Vaillancourt and his team a two-year, $855,000 grant to do the work.
“What’s not well understood is how the structure and function of the basal ganglia, or other parts of the brain, are affected early on in the disease,” said Vaillancourt.
He and his colleagues will recruit 25 subjects with early signs of Parkinson’s who haven’t yet begun taking drugs to control the disease. Their study will compare findings to a control group matched for age, gender and handedness — because all subjects will perform motor tasks with their hands while their brain is being imaged.
The study will be the first into early Parkinson’s to use functional brain imaging during gripping tasks designed to simulate everyday activities such as buttoning a shirt or blouse, or holding a cup.
“Individuals will undergo a brain scan while they exert force using their hands against a device that measures how hard and how fast they squeeze,” said Vaillancourt.
“Functional brain imaging will be targeted at the basal ganglia, which is the part of the brain that underlies symptoms of Parkinson’s disease.”
Vaillancourt’s group wants to study what is happening before Parkinson’s patients begin treatment with drugs such as levodopa that can change the way the brain functions. Pretreatment brain scans may be useful to develop markers for screening and diagnosis.
Those with Parkinson’s will be imaged as soon as possible after volunteering and will begin treatment with anti-Parkinson’s drugs afterward.
“With Parkinson’s, the brain must change over time, because it’s a neurodegenerative disease,” Vaillancourt said.
“This study will serve as the basis for trying to understand how the disease progresses.”
For more information go to www.parkinsonresearchfoundation.org
A research team from the University of Illinois at Chicago plans to use cutting-edge technology to study early-stage Parkinson’s disease.
They hope that tests using functional and high-resolution structural brain imaging will reveal new clues about early Parkinson’s disease.
Parkinson’s disease is a progressive, debilitating movement disorder pharmaceutically managed by using drugs that compensate for a lack of the neurotransmitter dopamine. Parkinson’s patients have a deficit of this important chemical because of degeneration in an area of the brain stem where it is made — a structure called the substantia nigra.
The National Institutes of Health has awarded David Vaillancourt and his team a two-year, $855,000 grant to do the work.
“What’s not well understood is how the structure and function of the basal ganglia, or other parts of the brain, are affected early on in the disease,” said Vaillancourt.
He and his colleagues will recruit 25 subjects with early signs of Parkinson’s who haven’t yet begun taking drugs to control the disease. Their study will compare findings to a control group matched for age, gender and handedness — because all subjects will perform motor tasks with their hands while their brain is being imaged.
The study will be the first into early Parkinson’s to use functional brain imaging during gripping tasks designed to simulate everyday activities such as buttoning a shirt or blouse, or holding a cup.
“Individuals will undergo a brain scan while they exert force using their hands against a device that measures how hard and how fast they squeeze,” said Vaillancourt.
“Functional brain imaging will be targeted at the basal ganglia, which is the part of the brain that underlies symptoms of Parkinson’s disease.”
Vaillancourt’s group wants to study what is happening before Parkinson’s patients begin treatment with drugs such as levodopa that can change the way the brain functions. Pretreatment brain scans may be useful to develop markers for screening and diagnosis.
Those with Parkinson’s will be imaged as soon as possible after volunteering and will begin treatment with anti-Parkinson’s drugs afterward.
“With Parkinson’s, the brain must change over time, because it’s a neurodegenerative disease,” Vaillancourt said.
“This study will serve as the basis for trying to understand how the disease progresses.”
For more information go to www.parkinsonresearchfoundation.org
Wednesday, November 4, 2009
Cholesterol-lowering drug could prevent Parkinson's
A commonly used cholesterol-lowering drug, called Simvastatin, can prevent progression of Parkinson's disease, according to a study by neurological Cholesterol-lowering drug could prevent Parkinson's researchers at Rush University Medical Center .
The study examined the use of the FDA-approved medication in mice with Parkinson’s disease and found that the drug successfully reverses the biochemical, cellular and anatomical changes caused by the disease.
"Statins are one of the most widely used cholesterol-lowering drugs throughout the world. This may be a safer approach to halt the disease progression in Parkinson’s patients," said study author Dr. Kalipada Pahan.
The researchers have shown that the activity of one protein called p21Ras is increased very early in the midbrain of mice with Parkinson’s pathology.
Simvastatin enters into the brain and blocks the activity of the p21Ras protein and other associated toxic molecules, and goes on to protect the neurons, normalize neurotransmitter levels, and improves the motor functions in the mice with Parkinson’s.
"Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of Parkinson’s. If we are able to replicate these results in Parkinson’s patients in the clinical setting, it would be a remarkable advance in the treatment of this devastating neurodegenerative disease," said Pahan.
For more information go to www.parkinsonresearchfoundation.org
The study examined the use of the FDA-approved medication in mice with Parkinson’s disease and found that the drug successfully reverses the biochemical, cellular and anatomical changes caused by the disease.
"Statins are one of the most widely used cholesterol-lowering drugs throughout the world. This may be a safer approach to halt the disease progression in Parkinson’s patients," said study author Dr. Kalipada Pahan.
The researchers have shown that the activity of one protein called p21Ras is increased very early in the midbrain of mice with Parkinson’s pathology.
Simvastatin enters into the brain and blocks the activity of the p21Ras protein and other associated toxic molecules, and goes on to protect the neurons, normalize neurotransmitter levels, and improves the motor functions in the mice with Parkinson’s.
"Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of Parkinson’s. If we are able to replicate these results in Parkinson’s patients in the clinical setting, it would be a remarkable advance in the treatment of this devastating neurodegenerative disease," said Pahan.
For more information go to www.parkinsonresearchfoundation.org
Tuesday, October 27, 2009
Health Talk: Correcting speech disorders associated with Parkinson's
By MARY MILLER
Parkinson's disease is the second most common neurological degenerative disorder. It is caused by a gradual loss of certain brain cells that produce dopamine, a chemical that helps muscles work properly. Without this chemical, problems with muscle movement occur.
Medications and surgical intervention can control and improve some of the symptoms experienced with walking, but there is not an effective solution to the speech or swallowing disorders that occur.
Since Parkinson's disease affects the nervous system and speech is driven by neurological functions, nearly every person diagnosed with Parkinson's disease will experience problems with their speech.
Speech problems from Parkinson's disease usually begin as a soft voice, mumbled or monotone speech and/or hoarseness. These problems start early and frequently affect quality of life. People are forced to withdraw from the workforce, limit their social activities and are usually asked to repeat themselves when communicating. The only way to improve speech that is altered from Parkinson's disease is with speech therapy.
The Lee Silverman Voice Treatment in an intense speech therapy program that was developed after more than 15 years of research. Patients attend therapy four times a week for four weeks and can only be administered by an LSVT certified speech therapist. Patients go througha series of exercises with the sole focus of producing a louder voice. After they are able to produce a louder voice they advance to practicing common phrases and sentences and onto conversations.
Patients are also required to practice daily, using the tailored home program provided by their therapist. Upon completion of therapy, patients will display improved voice intensity, improved intelligibility and increased facial expression. Some patients even report an improved swallowing function. The results of the treatment have been known to last for up to two years.
For more information go to www.parkinsonresearchfoundation.org
Parkinson's disease is the second most common neurological degenerative disorder. It is caused by a gradual loss of certain brain cells that produce dopamine, a chemical that helps muscles work properly. Without this chemical, problems with muscle movement occur.
Medications and surgical intervention can control and improve some of the symptoms experienced with walking, but there is not an effective solution to the speech or swallowing disorders that occur.
Since Parkinson's disease affects the nervous system and speech is driven by neurological functions, nearly every person diagnosed with Parkinson's disease will experience problems with their speech.
Speech problems from Parkinson's disease usually begin as a soft voice, mumbled or monotone speech and/or hoarseness. These problems start early and frequently affect quality of life. People are forced to withdraw from the workforce, limit their social activities and are usually asked to repeat themselves when communicating. The only way to improve speech that is altered from Parkinson's disease is with speech therapy.
The Lee Silverman Voice Treatment in an intense speech therapy program that was developed after more than 15 years of research. Patients attend therapy four times a week for four weeks and can only be administered by an LSVT certified speech therapist. Patients go througha series of exercises with the sole focus of producing a louder voice. After they are able to produce a louder voice they advance to practicing common phrases and sentences and onto conversations.
Patients are also required to practice daily, using the tailored home program provided by their therapist. Upon completion of therapy, patients will display improved voice intensity, improved intelligibility and increased facial expression. Some patients even report an improved swallowing function. The results of the treatment have been known to last for up to two years.
For more information go to www.parkinsonresearchfoundation.org
Monday, October 19, 2009
Acid associated with gout 'could help Parkinson's sufferers'
By Kate Devlin
Parkinson’s disease progresses more slowly in patients with naturally high levels of the acid which triggers gout, suggesting a possible new treatment for the disease.
Patients with high levels of uric acid were a third less likely to need treatment over the course of two years than those with low levels, the results of a new study show.
Researchers are now testing whether increasing Parkinson’s patients’ uric acid levels safely can help their condition.
An antioxidant, the acid is created naturally as we digest food.
But too much uric acid, or urate, can cause bouts of gout, an extremely painful joint condition, and kidney stones.
Diets rich in liver, seafood and dried beans have been linked to high uric acid levels but researchers warn that because of the side effects patients should not try to increase their urate levels themselves.
A smaller study published last year also suggested that high uric acid levels could slow the progression of Parkinson’s Disease.
Dr Alberto Ascherio, from the Harvard School of Public Health, who led the study, said: “Only now we can be reasonably sure that the slower rate of progression in patients with higher concentrations of urate is real and not a chance occurrence."
However, the researchers stress that they do not yet know if it is the acid itself which carries the protective benefit or some other process of the body which produces uric acid as a by-product.
The latest research looked at 800 sufferers of the condition.
The link between high uric acid levels and a slower development of the disease was less clear in women then men, the study found, however this may be because women tend to have higher natural levels of the acid.
About 120,000 people in Britain are thought to have the condition.
Famous sufferers include the actor Michael J Fox.
The researchers are now conducting a trial, sponsored by the Michael J Fox Foundation, to give 90 patients a drug, inosine, which can elevate uric acid levels, to test whether they can be safely raised and if this slows the speed of the disease.
"Because elevated urate levels have known health risks, including gout and kidney stones urate elevation should only be attempted in the context of a closely monitored clinical trial in which potential benefits and risks are carefully balanced," Dr Schwarzschild said.
For more information go to www.parkinsonresearchfoundation.org
Parkinson’s disease progresses more slowly in patients with naturally high levels of the acid which triggers gout, suggesting a possible new treatment for the disease.
Patients with high levels of uric acid were a third less likely to need treatment over the course of two years than those with low levels, the results of a new study show.
Researchers are now testing whether increasing Parkinson’s patients’ uric acid levels safely can help their condition.
An antioxidant, the acid is created naturally as we digest food.
But too much uric acid, or urate, can cause bouts of gout, an extremely painful joint condition, and kidney stones.
Diets rich in liver, seafood and dried beans have been linked to high uric acid levels but researchers warn that because of the side effects patients should not try to increase their urate levels themselves.
A smaller study published last year also suggested that high uric acid levels could slow the progression of Parkinson’s Disease.
Dr Alberto Ascherio, from the Harvard School of Public Health, who led the study, said: “Only now we can be reasonably sure that the slower rate of progression in patients with higher concentrations of urate is real and not a chance occurrence."
However, the researchers stress that they do not yet know if it is the acid itself which carries the protective benefit or some other process of the body which produces uric acid as a by-product.
The latest research looked at 800 sufferers of the condition.
The link between high uric acid levels and a slower development of the disease was less clear in women then men, the study found, however this may be because women tend to have higher natural levels of the acid.
About 120,000 people in Britain are thought to have the condition.
Famous sufferers include the actor Michael J Fox.
The researchers are now conducting a trial, sponsored by the Michael J Fox Foundation, to give 90 patients a drug, inosine, which can elevate uric acid levels, to test whether they can be safely raised and if this slows the speed of the disease.
"Because elevated urate levels have known health risks, including gout and kidney stones urate elevation should only be attempted in the context of a closely monitored clinical trial in which potential benefits and risks are carefully balanced," Dr Schwarzschild said.
For more information go to www.parkinsonresearchfoundation.org
Monday, October 5, 2009
Science News Share Blog Cite Print Email BookmarkCholesterol Necessary For Brain Development, Study Finds
ScienceDaily (Oct. 4, 2009)
A derivative of cholesterol is necessary for the formation of brain cells, according to a study from the Swedish medical university Karolinska Institutet. The results, which are published in the journal Cell Stem Cell, can help scientists to cultivate dopamine-producing cells outside the body.
The study was led by Professor Ernest Arenas and demonstrates that the formation of dopamine-producing neurons during brain development in mice is dependent on the activation of a specific receptor in the brain by an oxidised form of cholesterol called oxysterol. Dopamine-producing nerve cells play an important part in many brain functions and processes, from motor skills to reward systems and dependency. They are also the type of cell that dies in Parkinson's disease.
The scientists have also shown that embryonic stem cells cultivated in the laboratory, form more dopamine-producing nerve cells if they are treated with oxidised cholesterol. The same treatment also reduced the tendency of the stem cells to show uncontrolled growth.
"Oxysterol contributes to a safer and better cultivation of dopamine-producing cells, which is a great advancement since it increases the possibility of developing new treatments for Parkinsons disease," says Professor Arenas.
It is hoped that one day it will be possible to replace dead cells in the brains of Parkinson's patients with transplanted cultivated dopamine-producing cells. Such cells can also be used to test new Parkinson's drugs.
For more information go to www.parkinsonresearchfoundation.org
A derivative of cholesterol is necessary for the formation of brain cells, according to a study from the Swedish medical university Karolinska Institutet. The results, which are published in the journal Cell Stem Cell, can help scientists to cultivate dopamine-producing cells outside the body.
The study was led by Professor Ernest Arenas and demonstrates that the formation of dopamine-producing neurons during brain development in mice is dependent on the activation of a specific receptor in the brain by an oxidised form of cholesterol called oxysterol. Dopamine-producing nerve cells play an important part in many brain functions and processes, from motor skills to reward systems and dependency. They are also the type of cell that dies in Parkinson's disease.
The scientists have also shown that embryonic stem cells cultivated in the laboratory, form more dopamine-producing nerve cells if they are treated with oxidised cholesterol. The same treatment also reduced the tendency of the stem cells to show uncontrolled growth.
"Oxysterol contributes to a safer and better cultivation of dopamine-producing cells, which is a great advancement since it increases the possibility of developing new treatments for Parkinsons disease," says Professor Arenas.
It is hoped that one day it will be possible to replace dead cells in the brains of Parkinson's patients with transplanted cultivated dopamine-producing cells. Such cells can also be used to test new Parkinson's drugs.
For more information go to www.parkinsonresearchfoundation.org
Tuesday, September 22, 2009
Discovery could ‘protect brain cells from Parkinson’s’
A drug has been identified as a possible protector from Parkinson’s disease, according to a new study.
A drug more commonly dished out to transplant patients may be a good way at protecting brain cells from “rogue” genes which can lead to Parkinson’s disease, it is said.
Alex Whitworth and the team, based at the University of Sheffield, said that while rapamycin is no “wonder drug” for the treatment of the condition, the study proves that animal and human models that were used may be particularly valuable in discovering new drugs for directly treating the condition.
Dr Kieran Breen, who funded the work in his capacity as the director of research and development at the Parkinson’s Disease Society (PDS), explained: “It’s early days yet, and there’s a great deal of work to be done before we will know if these findings can be applied to all forms of Parkinson’s.
“But the discovery of this pathway may be the key to developing new drugs that could slow or even stop the progressive loss of nerve cells in the brain.”
In its capacity as a charitable force, the PDS announced last week that it is to donate £380,000 to the University of Edinburgh to understand the role of nerve cells in the progression of the condition.
For more information go to www.parkinsonresearchfoundation.org
A drug more commonly dished out to transplant patients may be a good way at protecting brain cells from “rogue” genes which can lead to Parkinson’s disease, it is said.
Alex Whitworth and the team, based at the University of Sheffield, said that while rapamycin is no “wonder drug” for the treatment of the condition, the study proves that animal and human models that were used may be particularly valuable in discovering new drugs for directly treating the condition.
Dr Kieran Breen, who funded the work in his capacity as the director of research and development at the Parkinson’s Disease Society (PDS), explained: “It’s early days yet, and there’s a great deal of work to be done before we will know if these findings can be applied to all forms of Parkinson’s.
“But the discovery of this pathway may be the key to developing new drugs that could slow or even stop the progressive loss of nerve cells in the brain.”
In its capacity as a charitable force, the PDS announced last week that it is to donate £380,000 to the University of Edinburgh to understand the role of nerve cells in the progression of the condition.
For more information go to www.parkinsonresearchfoundation.org
Monday, September 14, 2009
THE WORLD'S SMALLEST DEEP BRAIN STIMULATOR FOR PARKINSON'S DISEASE
11th September 2009 - News release
Approval has been given for the world's smallest, longest-lasting rechargeable Deep Brain Stimulator (DBS) for Parkinson's Disease. Deep Brain Stimulation (DBS) involves the use in Parkinson's Disease of electrodes that are implanted into the brain and connected to a small electrical device that can be externally programmed. For more information go to Deep brain stimulation. The new small device is called the Brio neurostimulator. It is very thin and light, and only slightly bigger than a man's wrist watch. Additionally, the device has the greatest recommended implant depth of any rechargeable DBS device. The thin profile and greater implant depth potentially makes the neurostimulator less noticeable and more comfortable for patients. The Brio DBS system delivers mild electrical pulses to specific targets in the brain, stimulating the structures that are involved in muscular movement. The system consists of a neurostimulator – a surgically implanted battery-operated device that generates the electrical pulses – and leads which carry the pulses to the brain to influence the irregular nerve signals responsible for the symptoms of Parkinson’s Disease.
For more information go to www.parkinsonresearchfoundation.org
Approval has been given for the world's smallest, longest-lasting rechargeable Deep Brain Stimulator (DBS) for Parkinson's Disease. Deep Brain Stimulation (DBS) involves the use in Parkinson's Disease of electrodes that are implanted into the brain and connected to a small electrical device that can be externally programmed. For more information go to Deep brain stimulation. The new small device is called the Brio neurostimulator. It is very thin and light, and only slightly bigger than a man's wrist watch. Additionally, the device has the greatest recommended implant depth of any rechargeable DBS device. The thin profile and greater implant depth potentially makes the neurostimulator less noticeable and more comfortable for patients. The Brio DBS system delivers mild electrical pulses to specific targets in the brain, stimulating the structures that are involved in muscular movement. The system consists of a neurostimulator – a surgically implanted battery-operated device that generates the electrical pulses – and leads which carry the pulses to the brain to influence the irregular nerve signals responsible for the symptoms of Parkinson’s Disease.
For more information go to www.parkinsonresearchfoundation.org
Sunday, September 6, 2009
Antibiotic can turn off transplanted genes in brain
A pair of genes transplanted into the brains of lab rats can lead to the production of a neurochemical that is in short supply in many people with Parkinson's disease.
But what happens if the irrevocable delivery of the genes goes bad and causes unwanted side effects?
That concern has been on the minds of researchers seeking ways to spur brain cells into producing the neurochemical, dopamine.
Scientists at the University of Florida say they may have an answer for transplanted genes that may have run amok.
In an article published in the online version of the journal Molecular Therapy, a team at UF's McKnight Brain Institute and Powell Gene Therapy Center report that a common antibiotic appears to be able to slow down or turn off the genes after they have been transplanted.
This could be significant, because the UF researchers think earlier experimental attempts using growth factors - naturally occurring substances that cause cells to grow and divide - to revive dying brain cells and get them to produce dopamine again may have failed because they occurred too late in the course of the disease.
Doctors would be reluctant to try the gene transplant technique for revitalizing dopamine production if it carried the risk of inflicting permanent negative side effects on people who are still relatively health because their Parkinson's disease is in early stages.
Ronald Mandel, a professor of neuroscience at UF, and his colleagues have been studying the use of a virus as a "vector" that delivers the genes needed to protect brain cells that produce dopamine.
"We have worked every day for 10 years to design a construct to the gene delivery vector that enhances the safety profile of gene transfer for Parkinson's disease," Mandel says.
In the technique the UF team has been exploring, the two transplanted genes must work together to produce the protein molecule that plays a key role in the process.
The researchers have now discovered that the antibiotic doxycycline, depending on the dose given, can slow down or turn off that protein production by the transplanted genes.
"With that added measure of safety, we believe we can intervene with gene transfer in patients at earlier stages of the disease," Mandel says.
Doxycycline, a member of the tetracycline class of antibiotics, is used to treat various forms of bacterial infection and acne.
If the UF researchers are right, this could be the first time scientists would be able to regulate a gene therapy after the treatment has been delivered.
"With this technique, you could adjust the therapy in the patient," said Fredric P. Manfredsson, a postdoctoral associate in UF's department of neuroscience. "That would be extremely helpful because no one is really certain yet what dosage is required for a protective effect in humans."
Being able to control gene regulation could help the development of safety gene therapies, according to Mark Tuszynski, a professor of neurosciences and director of the Center for Neural Repair at the University of California, San Diego.
"The work of Dr. Mandel and colleagues brings us an important step closer to this goal," says Tuszynski, who had no involvement in the UF research
For more information go to: www.parkinsonresearchfoundation.org
But what happens if the irrevocable delivery of the genes goes bad and causes unwanted side effects?
That concern has been on the minds of researchers seeking ways to spur brain cells into producing the neurochemical, dopamine.
Scientists at the University of Florida say they may have an answer for transplanted genes that may have run amok.
In an article published in the online version of the journal Molecular Therapy, a team at UF's McKnight Brain Institute and Powell Gene Therapy Center report that a common antibiotic appears to be able to slow down or turn off the genes after they have been transplanted.
This could be significant, because the UF researchers think earlier experimental attempts using growth factors - naturally occurring substances that cause cells to grow and divide - to revive dying brain cells and get them to produce dopamine again may have failed because they occurred too late in the course of the disease.
Doctors would be reluctant to try the gene transplant technique for revitalizing dopamine production if it carried the risk of inflicting permanent negative side effects on people who are still relatively health because their Parkinson's disease is in early stages.
Ronald Mandel, a professor of neuroscience at UF, and his colleagues have been studying the use of a virus as a "vector" that delivers the genes needed to protect brain cells that produce dopamine.
"We have worked every day for 10 years to design a construct to the gene delivery vector that enhances the safety profile of gene transfer for Parkinson's disease," Mandel says.
In the technique the UF team has been exploring, the two transplanted genes must work together to produce the protein molecule that plays a key role in the process.
The researchers have now discovered that the antibiotic doxycycline, depending on the dose given, can slow down or turn off that protein production by the transplanted genes.
"With that added measure of safety, we believe we can intervene with gene transfer in patients at earlier stages of the disease," Mandel says.
Doxycycline, a member of the tetracycline class of antibiotics, is used to treat various forms of bacterial infection and acne.
If the UF researchers are right, this could be the first time scientists would be able to regulate a gene therapy after the treatment has been delivered.
"With this technique, you could adjust the therapy in the patient," said Fredric P. Manfredsson, a postdoctoral associate in UF's department of neuroscience. "That would be extremely helpful because no one is really certain yet what dosage is required for a protective effect in humans."
Being able to control gene regulation could help the development of safety gene therapies, according to Mark Tuszynski, a professor of neurosciences and director of the Center for Neural Repair at the University of California, San Diego.
"The work of Dr. Mandel and colleagues brings us an important step closer to this goal," says Tuszynski, who had no involvement in the UF research
For more information go to: www.parkinsonresearchfoundation.org
Sunday, August 30, 2009
Finnish scientists discover nerve growth factor with therapeutic potential in Parkinson's disease
Scientists in the Academy of Finland's Neuroscience Research Programme have reported promising new results with potential implications for the treatment of Parkinson's disease. They have been studying the impacts of nerve growth factors in the treatment of PD, and their latest results show that a certain growth factor can be used to halt the progress of damage brought on by a nerve poison and possibly even restore the function of damaged cells.
The studies on nerve growth factors used an experimental PD model in rats. Administration of the growth factor reduced motor disturbances in rats.
The severe motor disturbances that are seen in PD are caused by the slow degeneration of dopamine nerves in the brain. There are treatments that alleviate the symptoms of the disease, such as hand tremor, but they do not prevent or halt the degeneration of nerve cells. The nerve growth factors studied to date have slowed nerve cell degeneration to some extent, but they have had only limited therapeutic effect. Several known nerve growth factors, such as GDNF, also attach to extracellular tissue, possibly deterring their movement to nerve cells that require treatment.
Working under the supervision of Academy Professor Mart Saarma, scientists at the University of Helsinki Institute of Biotechnology have now been investigating two new nerve growth factors. MANF (mesencephalic astrocyte-derived neurotrophic factor) is released from glial cells in the midbrain and is a member of the same growth factor family as CDNF, another growth factor that Saarma's team have investigated. A University of Helsinki team led by Professor Raimo K. Tuominen discovered that in the experimental PD model, MANF and CDNF injections into the brain prevented dopamine nerve destruction caused by nerve poison and to some extent even restored the function of damaged cells in rats.
The latest results suggest that MANF spreads more readily in brain tissue than other known growth factors. This may be a highly significant finding in respect to the development of growth factor therapy for PD.
The studies on nerve growth factors used an experimental PD model in rats. Administration of the growth factor reduced motor disturbances in rats.
The severe motor disturbances that are seen in PD are caused by the slow degeneration of dopamine nerves in the brain. There are treatments that alleviate the symptoms of the disease, such as hand tremor, but they do not prevent or halt the degeneration of nerve cells. The nerve growth factors studied to date have slowed nerve cell degeneration to some extent, but they have had only limited therapeutic effect. Several known nerve growth factors, such as GDNF, also attach to extracellular tissue, possibly deterring their movement to nerve cells that require treatment.
Working under the supervision of Academy Professor Mart Saarma, scientists at the University of Helsinki Institute of Biotechnology have now been investigating two new nerve growth factors. MANF (mesencephalic astrocyte-derived neurotrophic factor) is released from glial cells in the midbrain and is a member of the same growth factor family as CDNF, another growth factor that Saarma's team have investigated. A University of Helsinki team led by Professor Raimo K. Tuominen discovered that in the experimental PD model, MANF and CDNF injections into the brain prevented dopamine nerve destruction caused by nerve poison and to some extent even restored the function of damaged cells in rats.
The latest results suggest that MANF spreads more readily in brain tissue than other known growth factors. This may be a highly significant finding in respect to the development of growth factor therapy for PD.
Monday, July 20, 2009
Initial treatment for Parkinson's disease
No known treatment can stop or reverse the breakdown of nerve cells that causes Parkinson's disease. However, drugs can relieve many symptoms of the disease. Surgery also can be effective in a small number of people to treat symptoms of Parkinson's disease.
Treatment is different for every person, and the type of treatment you will need may change as the disease progresses. Your age, work status, family, and living situation can all affect decisions about when to begin treatment, what types of treatment to use, and when to make changes in treatment. As your medical condition changes, you may need regular adjustments in your treatment to balance quality-of-life issues, side effects of treatment, and treatment costs.
Parkinson's disease causes a wide range of symptoms and complications. This topic covers the overall management of the disease. This topic does not discuss managing specific symptoms.
Initial treatment
If your symptoms are mild, you may not need treatment for Parkinson's disease. Your doctor may wait to prescribe treatment with drugs until your symptoms begin to interfere with your daily activities. Additional treatment methods (such as exercise, physical therapy, and occupational therapy) can be helpful at all stages of Parkinson's disease to help you maintain your strength, mobility, and independence.
If you do need drugs at this point, there are several options. Levodopa is considered the "gold standard" of treatment for Parkinson's disease. But levodopa can have negative effects when used long-term. Because of this, dopamine agonists such as pramipexole and ropinirole often are used first. Other non-dopamine drugs may be used early in the course of the disease. These include amantadine, monoamine oxidase inhibitors (such as selegiline), and anticholinergics (such as trihexyphenidyl). As the disease progresses, levodopa will likely need to be added.
Early in the disease, it might be helpful to take pills with food to help with nausea, which may be caused by some medicines taken for Parkinson's disease. Later in the disease, taking the medicines at least one hour before meals (and at least two hours after meals) may help them work better.
Your doctor, other health professionals, or Parkinson's disease support groups can help you get emotional support and education about the illness. This is important both early and throughout the course of the disease.
Ongoing treatment
As Parkinson's disease progresses, the symptoms usually become more disabling. Most people develop mild to moderate tremor. Movement is often slow and limited due to muscular rigidity and the slowing down and loss of automatic and spontaneous movement (bradykinesia). Treatment in this stage is determined by weighing the severity of the symptoms against the side effects of drugs.
The symptoms of Parkinson's disease change as the disease progresses. Because of this, your doctor will adjust your drugs to deal with the symptoms as they appear. Levodopa is the most commonly used drug for Parkinson's disease. However, it may cause side effects with prolonged use or high dosages. Your doctor may prescribe dopamine agonists such as pramipexole or ropinirole to delay the point at which you need to begin taking levodopa. Studies have suggested that this may delay the onset of levodopa's side effects.234 Your doctor may also prescribe levodopa along with a dopamine agonist.
Treatment is different for every person, and the type of treatment you will need may change as the disease progresses. Your age, work status, family, and living situation can all affect decisions about when to begin treatment, what types of treatment to use, and when to make changes in treatment. As your medical condition changes, you may need regular adjustments in your treatment to balance quality-of-life issues, side effects of treatment, and treatment costs.
Parkinson's disease causes a wide range of symptoms and complications. This topic covers the overall management of the disease. This topic does not discuss managing specific symptoms.
Initial treatment
If your symptoms are mild, you may not need treatment for Parkinson's disease. Your doctor may wait to prescribe treatment with drugs until your symptoms begin to interfere with your daily activities. Additional treatment methods (such as exercise, physical therapy, and occupational therapy) can be helpful at all stages of Parkinson's disease to help you maintain your strength, mobility, and independence.
If you do need drugs at this point, there are several options. Levodopa is considered the "gold standard" of treatment for Parkinson's disease. But levodopa can have negative effects when used long-term. Because of this, dopamine agonists such as pramipexole and ropinirole often are used first. Other non-dopamine drugs may be used early in the course of the disease. These include amantadine, monoamine oxidase inhibitors (such as selegiline), and anticholinergics (such as trihexyphenidyl). As the disease progresses, levodopa will likely need to be added.
Early in the disease, it might be helpful to take pills with food to help with nausea, which may be caused by some medicines taken for Parkinson's disease. Later in the disease, taking the medicines at least one hour before meals (and at least two hours after meals) may help them work better.
Your doctor, other health professionals, or Parkinson's disease support groups can help you get emotional support and education about the illness. This is important both early and throughout the course of the disease.
Ongoing treatment
As Parkinson's disease progresses, the symptoms usually become more disabling. Most people develop mild to moderate tremor. Movement is often slow and limited due to muscular rigidity and the slowing down and loss of automatic and spontaneous movement (bradykinesia). Treatment in this stage is determined by weighing the severity of the symptoms against the side effects of drugs.
The symptoms of Parkinson's disease change as the disease progresses. Because of this, your doctor will adjust your drugs to deal with the symptoms as they appear. Levodopa is the most commonly used drug for Parkinson's disease. However, it may cause side effects with prolonged use or high dosages. Your doctor may prescribe dopamine agonists such as pramipexole or ropinirole to delay the point at which you need to begin taking levodopa. Studies have suggested that this may delay the onset of levodopa's side effects.234 Your doctor may also prescribe levodopa along with a dopamine agonist.
Monday, July 13, 2009
Oxford Biomedica says study of ProSavin Parkinson’s treatment progressing well
Gene therapy group Oxford Biomedica PLC (AIM: OXB) said the Phase I/II study of its novel gene therapy, ProSavin, for the treatment of Parkinson's disease is progressing well.
Patients treated at the first dose level have maintained their improvement in motor function for one year, with an average improvement of 29 percent. Analogous investigator assessments of patients in the second cohort treated at a higher dose level have achieved similar benefit at three months, and the first patient to reach their six-month assessment has demonstrated further improvement.
The independent data monitoring committee supported Oxford BioMedica's proposal to proceed to a third dose level incorporating the company's new administration technology.
The ongoing Phase I/II study is designed to evaluate the safety and efficacy of ProSavin in patients with mid-stage Parkinson's disease who are experiencing reduced benefit on L-DOPA 'equivalent' therapy.
ProSavin is administered directly into the striatum of the brain using a well established surgical technique. The first stage of the study is a dose escalation in cohorts of three patients at each dose level and, to date, six patients have been treated.
ProSavin has been safe and well tolerated in all patients, with no serious adverse events and no evidence of immunotoxicity. All patients have reduced or maintained their PD medication relative to baseline.
The monitoring committee supports the company's proposal to proceed directly to a third dose level that is five-fold higher than the first dose level. Oxford Biomedica will incorporate its new delivery technology for the administration of the 5x dose level of ProSavin.
The new technique reduces the surgical time, facilitates higher dosing and has the potential to provide better reproducibility as study centres expand and thus accelerate clinical development timelines. A protocol amendment for the new technology is being prepared, which it plans to submit to French healthcare regulatory agency, AFSSAPS, before the end of the third quarter of 2009.
Patients treated at the first dose level have maintained their improvement in motor function for one year, with an average improvement of 29 percent. Analogous investigator assessments of patients in the second cohort treated at a higher dose level have achieved similar benefit at three months, and the first patient to reach their six-month assessment has demonstrated further improvement.
The independent data monitoring committee supported Oxford BioMedica's proposal to proceed to a third dose level incorporating the company's new administration technology.
The ongoing Phase I/II study is designed to evaluate the safety and efficacy of ProSavin in patients with mid-stage Parkinson's disease who are experiencing reduced benefit on L-DOPA 'equivalent' therapy.
ProSavin is administered directly into the striatum of the brain using a well established surgical technique. The first stage of the study is a dose escalation in cohorts of three patients at each dose level and, to date, six patients have been treated.
ProSavin has been safe and well tolerated in all patients, with no serious adverse events and no evidence of immunotoxicity. All patients have reduced or maintained their PD medication relative to baseline.
The monitoring committee supports the company's proposal to proceed directly to a third dose level that is five-fold higher than the first dose level. Oxford Biomedica will incorporate its new delivery technology for the administration of the 5x dose level of ProSavin.
The new technique reduces the surgical time, facilitates higher dosing and has the potential to provide better reproducibility as study centres expand and thus accelerate clinical development timelines. A protocol amendment for the new technology is being prepared, which it plans to submit to French healthcare regulatory agency, AFSSAPS, before the end of the third quarter of 2009.
Saturday, June 13, 2009
Treatments and drugs
Your initial response to Parkinson's treatment can be dramatic. Over time, however, the benefits of drugs frequently diminish or become less consistent, although symptoms can usually still be fairly well controlled. Your doctor may recommend lifestyle changes, such as physical therapy, a healthy diet and exercise, in addition to medications. In some cases, surgery may be helpful.
Medications
Medications can help manage problems with walking, movement and tremor by increasing the brain's supply of dopamine. Taking dopamine itself is not helpful, because it is unable to enter your brain.
*
Levodopa. The most effective Parkinson's drug is levodopa, which is a natural substance that we all have in our body. When taken by mouth in pill form, it passes into the brain and is converted to dopamine. Levodopa is combined with carbidopa to create the combination drug Sinemet. The carbidopa protects levodopa from premature conversion to dopamine outside the brain; in doing that, it also prevents nausea. In Europe, levodopa is combined with a similar substance, benserazide, and is marketed as Madopar.
As the disease progresses, the benefit from levodopa may become less stable, with a tendency to wax and wane ("wearing off"). This then requires medication adjustments. Levodopa side effects include confusion, delusions and hallucinations, as well as involuntary movements called dyskinesia. These resolve with dose reduction, but sometimes at the expense of reduced parkinsonism control.
*
Dopamine agonists. Unlike levodopa, these drugs aren't changed into dopamine. Instead, they mimic the effects of dopamine in the brain and cause neurons to react as though dopamine is present. They are not nearly as effective in treating the symptoms of Parkinson's disease. However, they last longer and are often used to smooth the sometimes off-and-on effect of levodopa.
This class includes pill forms of dopamine agonists, pramipexole (Mirapex) and ropinirole (Requip), as well as a patch form, rotigotine (Neupro). Pergolide (Permax) has been withdrawn from the market because of its association with heart valve problems. A short-acting injectable dopamine agonist, apomorphine (Apokyn), is used for quick relief.
The side effects of dopamine agonists include those of carbidopa-levodopa, although they're less likely to cause involuntary movements. However, they are substantially more likely to cause hallucinations, sleepiness or swelling. These medications may also increase your risk of compulsive behaviors such as hypersexuality, compulsive gambling and compulsive overeating. If you are taking these medications and start behaving in a way that's out of character for you, talk to your doctor.
* MAO B inhibitors. These types of drugs, including selegiline (Eldepryl) and rasagiline (Azilect), help prevent the breakdown of both naturally occurring dopamine and dopamine formed from levodopa. They do this by inhibiting the activity of the enzyme monoamine oxidase B (MAO B) — the enzyme that metabolizes dopamine in the brain. Side effects are rare but can include serious interactions with other medications, including drugs to treat depression and certain narcotics.
* Catechol O-methyltransferase (COMT) inhibitors. These drugs prolong the effect of carbidopa-levodopa therapy by blocking an enzyme that breaks down levodopa. Tolcapone (Tasmar) has been linked to liver damage and liver failure, so it's normally used only in people who aren't responding to other therapies. Entacapone (Comtan) doesn't cause liver problems and is now combined with carbidopa and levodopa in a medication called Stalevo.
* Anticholinergics. These drugs have been used for many years to help control the tremor associated with Parkinson's disease. A number of anticholinergic drugs, such as trihexyphenidyl and benztropine (Cogentin), are available. However, their modest benefits may be offset by side effects such as confusion and hallucinations, particularly in people over the age of 70. Other side effects include dry mouth, nausea, urine retention — especially in men with an enlarged prostate — and severe constipation.
* Antivirals. Doctors may prescribe amantadine (Symmetrel) alone to provide short-term relief of mild, early-stage Parkinson's disease. It also may be added to carbidopa-levodopa therapy for people in the later stages of Parkinson's disease, especially if they have problems with involuntary movements (dyskinesia) induced by carbidopa-levodopa. Side effects include swollen ankles and a purple mottling of the skin.
Physical therapy
Exercise is important for general health, but especially for maintaining function in Parkinson's disease. Physical therapy may be advisable and can help improve mobility, range of motion and muscle tone. Although specific exercises can't stop the progress of the disease, improving muscle strength can help you feel more confident and capable. A physical therapist can also work with you to improve your gait and balance. A speech therapist or speech pathologist can improve problems with speaking and swallowing.
Surgery
Deep brain stimulation is the most common surgical procedure to treat Parkinson's disease. It involves implanting an electrode deep within the parts of your brain that control movement. The amount of stimulation delivered by the electrode is controlled by a pacemaker-like device placed under the skin in your upper chest. A wire that travels under your skin connects the device, called a pulse generator, to the electrode.
Deep brain stimulation is most often used for people who have advanced Parkinson's disease who have unstable medication (levodopa) responses. It can stabilize medication fluctuations and reduce or eliminate involuntary movements (dyskinesias). Tremor is especially responsive to this therapy. Deep brain stimulation doesn't help dementia and may make that worse.
Like any other brain surgery, this procedure has risks — such as brain hemorrhage or stroke-like problems. Infection also may occur, requiring parts of the device to be replaced. In addition, the unit's battery beneath the skin of the chest wall must be surgically replaced every few years. Deep brain stimulation isn't beneficial for people who don't respond to carbidopa-levodopa.
Medications
Medications can help manage problems with walking, movement and tremor by increasing the brain's supply of dopamine. Taking dopamine itself is not helpful, because it is unable to enter your brain.
*
Levodopa. The most effective Parkinson's drug is levodopa, which is a natural substance that we all have in our body. When taken by mouth in pill form, it passes into the brain and is converted to dopamine. Levodopa is combined with carbidopa to create the combination drug Sinemet. The carbidopa protects levodopa from premature conversion to dopamine outside the brain; in doing that, it also prevents nausea. In Europe, levodopa is combined with a similar substance, benserazide, and is marketed as Madopar.
As the disease progresses, the benefit from levodopa may become less stable, with a tendency to wax and wane ("wearing off"). This then requires medication adjustments. Levodopa side effects include confusion, delusions and hallucinations, as well as involuntary movements called dyskinesia. These resolve with dose reduction, but sometimes at the expense of reduced parkinsonism control.
*
Dopamine agonists. Unlike levodopa, these drugs aren't changed into dopamine. Instead, they mimic the effects of dopamine in the brain and cause neurons to react as though dopamine is present. They are not nearly as effective in treating the symptoms of Parkinson's disease. However, they last longer and are often used to smooth the sometimes off-and-on effect of levodopa.
This class includes pill forms of dopamine agonists, pramipexole (Mirapex) and ropinirole (Requip), as well as a patch form, rotigotine (Neupro). Pergolide (Permax) has been withdrawn from the market because of its association with heart valve problems. A short-acting injectable dopamine agonist, apomorphine (Apokyn), is used for quick relief.
The side effects of dopamine agonists include those of carbidopa-levodopa, although they're less likely to cause involuntary movements. However, they are substantially more likely to cause hallucinations, sleepiness or swelling. These medications may also increase your risk of compulsive behaviors such as hypersexuality, compulsive gambling and compulsive overeating. If you are taking these medications and start behaving in a way that's out of character for you, talk to your doctor.
* MAO B inhibitors. These types of drugs, including selegiline (Eldepryl) and rasagiline (Azilect), help prevent the breakdown of both naturally occurring dopamine and dopamine formed from levodopa. They do this by inhibiting the activity of the enzyme monoamine oxidase B (MAO B) — the enzyme that metabolizes dopamine in the brain. Side effects are rare but can include serious interactions with other medications, including drugs to treat depression and certain narcotics.
* Catechol O-methyltransferase (COMT) inhibitors. These drugs prolong the effect of carbidopa-levodopa therapy by blocking an enzyme that breaks down levodopa. Tolcapone (Tasmar) has been linked to liver damage and liver failure, so it's normally used only in people who aren't responding to other therapies. Entacapone (Comtan) doesn't cause liver problems and is now combined with carbidopa and levodopa in a medication called Stalevo.
* Anticholinergics. These drugs have been used for many years to help control the tremor associated with Parkinson's disease. A number of anticholinergic drugs, such as trihexyphenidyl and benztropine (Cogentin), are available. However, their modest benefits may be offset by side effects such as confusion and hallucinations, particularly in people over the age of 70. Other side effects include dry mouth, nausea, urine retention — especially in men with an enlarged prostate — and severe constipation.
* Antivirals. Doctors may prescribe amantadine (Symmetrel) alone to provide short-term relief of mild, early-stage Parkinson's disease. It also may be added to carbidopa-levodopa therapy for people in the later stages of Parkinson's disease, especially if they have problems with involuntary movements (dyskinesia) induced by carbidopa-levodopa. Side effects include swollen ankles and a purple mottling of the skin.
Physical therapy
Exercise is important for general health, but especially for maintaining function in Parkinson's disease. Physical therapy may be advisable and can help improve mobility, range of motion and muscle tone. Although specific exercises can't stop the progress of the disease, improving muscle strength can help you feel more confident and capable. A physical therapist can also work with you to improve your gait and balance. A speech therapist or speech pathologist can improve problems with speaking and swallowing.
Surgery
Deep brain stimulation is the most common surgical procedure to treat Parkinson's disease. It involves implanting an electrode deep within the parts of your brain that control movement. The amount of stimulation delivered by the electrode is controlled by a pacemaker-like device placed under the skin in your upper chest. A wire that travels under your skin connects the device, called a pulse generator, to the electrode.
Deep brain stimulation is most often used for people who have advanced Parkinson's disease who have unstable medication (levodopa) responses. It can stabilize medication fluctuations and reduce or eliminate involuntary movements (dyskinesias). Tremor is especially responsive to this therapy. Deep brain stimulation doesn't help dementia and may make that worse.
Like any other brain surgery, this procedure has risks — such as brain hemorrhage or stroke-like problems. Infection also may occur, requiring parts of the device to be replaced. In addition, the unit's battery beneath the skin of the chest wall must be surgically replaced every few years. Deep brain stimulation isn't beneficial for people who don't respond to carbidopa-levodopa.
Saturday, June 6, 2009
Creatine and Possible Benefits to Parkinson’s Disease Victims
Creatine, also known as creatine monohydrate, creatine phosphate or creatine citrate, is a naturally occurring amino acid compound in your body that is made by your liver and facilitates the production of energy in your body. Most of the creatine is stored in your skeletal muscles and the rest is found in your brain, heart and testes. You can eat foods that have creatine, such as red meat and fish. However, creatine is also available in supplement form through health food and drug stores.
Promoted in supplement form as an energy enhancement, creatine use is encouraged by the exercise and bodybuilding industries to increase exercise performance. It is this long-standing benefit that has lead scientists to organize large-scale national clinical trials of the product to determine if creatine can have a beneficial effect on symptoms of Parkinson’s disease. Classified by the Food and Drug Administration (FDA) as a nutritional supplement, creatine is widely used by professional athletes and is considered safe for daily supplemental use.
Researchers have also concluded that creatine increases the available energy for brain nerve cells and that this process helps prevent the loss of mitochondria. As a result it has positive effect on the health and survival of your nerve cell. Recognizing that an increase in cellular energy is beneficial to the health of your nerve cells, researchers believe that the addition of creatine to the diet will prevent injury and the premature death of the neurotransmitters and cells of your brain that are affected by Parkinson’s disease.
The symptoms of Parkinson’s, progressively uncontrollable shaking of the limbs and degeneration in the ability to speak, result from a reduction of dopamine in the brain. Dopamine is a neurotransmitter, which helps control movement. It is the hope of researchers that the introduction of creatine will increase the neurological response between brain cells and result in a potential treatment for the sufferers of Parkinson’s disease.
In prior 18 month clinical trials of several potential Parkinson’s treatments, in which the trials were designed to eliminate those that are proven to be futile, results indicated that creatine being noted as warranting of further large scale clinical study for efficacy. Researchers also noted that creatine was well tolerated by test subjects. Prior research on creatine, unrelated to study of Parkinson’s disease or its treatment, have also resulted in no long term or serious side effects.
The research studies to determine whether creatine will be instrumental in arresting the progression of Parkinson’s disease will last for 5 to 7 years. The subjects will be those that have been diagnosed with Parkinson’s in the last five years and have been treated for two years or less with drugs that increase the levels of dopamine in the brain. Additional benefits of creatine, which have researchers optimistic in the study outcome, include its antioxidant properties that have been shown to prevent brain cell loss in laboratory mice that are affected with Parkinson’s disease. Researchers are encouraged by this revelation, and hope to prove the same effects of creatine to be present in human test subjects.
Promoted in supplement form as an energy enhancement, creatine use is encouraged by the exercise and bodybuilding industries to increase exercise performance. It is this long-standing benefit that has lead scientists to organize large-scale national clinical trials of the product to determine if creatine can have a beneficial effect on symptoms of Parkinson’s disease. Classified by the Food and Drug Administration (FDA) as a nutritional supplement, creatine is widely used by professional athletes and is considered safe for daily supplemental use.
Researchers have also concluded that creatine increases the available energy for brain nerve cells and that this process helps prevent the loss of mitochondria. As a result it has positive effect on the health and survival of your nerve cell. Recognizing that an increase in cellular energy is beneficial to the health of your nerve cells, researchers believe that the addition of creatine to the diet will prevent injury and the premature death of the neurotransmitters and cells of your brain that are affected by Parkinson’s disease.
The symptoms of Parkinson’s, progressively uncontrollable shaking of the limbs and degeneration in the ability to speak, result from a reduction of dopamine in the brain. Dopamine is a neurotransmitter, which helps control movement. It is the hope of researchers that the introduction of creatine will increase the neurological response between brain cells and result in a potential treatment for the sufferers of Parkinson’s disease.
In prior 18 month clinical trials of several potential Parkinson’s treatments, in which the trials were designed to eliminate those that are proven to be futile, results indicated that creatine being noted as warranting of further large scale clinical study for efficacy. Researchers also noted that creatine was well tolerated by test subjects. Prior research on creatine, unrelated to study of Parkinson’s disease or its treatment, have also resulted in no long term or serious side effects.
The research studies to determine whether creatine will be instrumental in arresting the progression of Parkinson’s disease will last for 5 to 7 years. The subjects will be those that have been diagnosed with Parkinson’s in the last five years and have been treated for two years or less with drugs that increase the levels of dopamine in the brain. Additional benefits of creatine, which have researchers optimistic in the study outcome, include its antioxidant properties that have been shown to prevent brain cell loss in laboratory mice that are affected with Parkinson’s disease. Researchers are encouraged by this revelation, and hope to prove the same effects of creatine to be present in human test subjects.
Saturday, May 30, 2009
Deep Brain Stimulation
Under the skin, a battery is surgically implanted -- generally within the upper chest. From the battery, wires snake up to the head, to tickle different targets deep inside the brain.
Such is the hardware for deep brain stimulation -- the equivalent of a cardiac pacemaker for the mind.
Until recently, deep brain stimulation was approved in the U.S. only to treat certain movement disorders, primarily those of Parkinson's disease, for which it diminishes tremors and rigidity and improves mobility. To date, more than 60,000 patients worldwide have had the devices implanted.
But now use of the technique seems set to mushroom.
This year, the Food and Drug Administration granted a so-called humanitarian device exemption for the treatment to be used in severe cases of obsessive-compulsive disorder -- the first approval of deep brain stimulation therapy for any psychiatric condition.
Large clinical trials are also in the works for use of deep brain stimulation for epilepsy and depression, and experimental studies in the U.S. and elsewhere -- still in their early stages -- are exploring the treatment for obesity, traumatic brain injury, severe chronic pain, Alzheimer's disease, anorexia, tinnitus and addiction.
There are discussions too on the possible use of deep brain stimulation to treat hypertension.
"The field is taking off," says Dr. Ali Rezai, director of functional neurosurgery at the Cleveland Clinic, who has been involved in research on movement disorders, traumatic brain injury, obsessive-compulsive disorder and severe depression, among others.
Some researchers warn, however, that with all this activity -- pushed in part by the industry that makes the brain-stimulation devices -- the field may be moving too fast.
"There is so much progress that's been made and so much potential -- you would hate to lose that potential," says Dr. Joseph Fins, chief of the division of medical ethics and a professor at Weill Cornell Medical College in New York.
Here's a look at deep brain stimulation as it moves beyond Parkinson's disease. (See the related story about reservations scientists have about the growth of the field, and go online at latimes.com/health for a look at less-explored applications such as traumatic brain injury and obesity.)
Obsessive- compulsive disorder
In studies with a total of 26 patients with severe obsessive-compulsive disorder, 60% of those whose device was turned on demonstrated "very much improved" symptoms after months of deep brain stimulation as measured by interviews and questionnaires, says Dr. Benjamin Greenberg, an associate professor at Brown University Medical School and Butler Hospital in Providence, R.I., who was one of the study researchers.
The patients had previously failed on medicines as well as behavioral cognitive therapy.
Yet the data, published last year in Molecular Psychiatry, can't really nail the effect of the treatment, Greenberg says, because the patients for the most part knew whether their devices were turned on or off. Thus, researchers can't rule out that some of the observed improvements were due to a placebo effect.
Patients were stimulated in an area called ventral capsule/ventral striatum, chosen, in part, because removal of nerve fibers in that area is known to cause improvement in obsessive-compulsive symptoms.
Based largely on these findings, the FDA recently granted a limited humanitarian device exemption that permits the device to be used in as many as 4,000 of the country's most severe cases of obsessive compulsive disorder per year.
To get this kind of exemption, Medtronic -- makers of the only deep brain stimulation device that is FDA-approved -- needed only to show its safety and probable benefit.
Greenberg is now doing a randomized, double-blinded trial with 30 patients, some of whom have devices turned on right away and some who have them turned on after a delay. No one will know whose device is turned on for the first several months of the trial.
Medtronic has conducted a large-scale randomized trial for deep brain stimulation on epilepsy. Data will be submitted to the FDA this year, says Paul Stypulkowski, senior director of therapy research of Medtronic.
The device was turned on, for three months, in half of the 110 volunteers, stimulating -- and thereby, paradoxically, inhibiting-- an area called the anterior nucleus of the thalamus. That area is believed to influence a circuit involved in seizures.
The data, presented in December at a meeting in Seattle, show that deep brain stimulation reduced the number of seizures by 38% compared with what was seen before implanting the device.
That is slightly better than improvement seen with vagus nerve stimulation, another FDA-approved electrical stimulation treatment, which reduces seizures by about 25%.
The control group whose device was kept turned off, also improved, by 14.5%. That could be due to a placebo effect. Or it might be because people who join trials are usually at their worst -- and often tend to improve somewhat on their own, says trial researcher Dr. Douglas Labar, of the Weill Cornell Medical College in New York.
If deep brain stimulation is approved, Labar says, patients will have the choice between a more efficient but also more risky treatment and the slightly less efficient but also less risky vagus nerve stimulation.
Depression
Medtronic and a second company, St. Paul, Minn.-based St. Jude Medical, have two large-scale randomized trials underway for severe, treatment-resistant depression. (St. Jude Medical recently received approval to sell its device for the treatment of Parkinson's disease in Europe and is now completing studies aimed at securing FDA approval for treating Parkinson's and another movement disorder in the U.S.)
Medtronic's depression trial will follow about 200 patients stimulated in an area called the anterior limb of the internal capsule for at least one year.
This brain target for depression was identified by accident: When obsessive-compulsive disorder patients who also had depression were stimulated in this area, their depression also improved.
In one case, a patient produced a one-sided smile when stimulated on one side of the brain and also expressed feelings of happiness, says study researcher Dr. Wayne Goodman of the National Institute of Mental Health.
In a recently published unblinded study, about half of 15 patients showed at least a 50% improvement in severe depression symptoms a year or more after surgery when the anterior limb of the internal capsule was stimulated, says Rezai, who was involved in the study.
St. Jude Medical chose a different brain target, area 25, for its depression trial, which will enroll more than 100 patients. Brain imaging studies have shown that area 25 is more active in depressed people.
In a study of 20 patients, 55% still responded to treatment as late as one year after surgery, says study author Dr. Helen Mayberg, professor of psychiatry and neurology at Emory University. That is an "unheard-of response rate" given that these patients had tried and failed every other treatment, including several medications and electroconvulsive therapy, Mayberg says.
By comparison, Mayberg says, stimulation of the vagus nerve in the neck, approved by the FDA for depression, has only a 15% response rate at 10 weeks in similarly severely depressed patients.
Dr. Thomas Schlaepfer, vice chairman of the department of psychiatry of the University of Bonn in Germany, has been treating severely depressed patients by stimulating yet a third brain target, the nucleus accumbens.
The nucleus accumbens doesn't show normal activity in depressed patients, which could explain why they are less able to experience pleasure.
Last year, Schlaepfer showed that deep brain stimulation in this area led to acute improvements in three severely depressed patients. He says he has extended the work to 10 patients, half of whom showed an improvement when examined a year later.
With deep brain stimulation now being tried in at least three brain areas for depression, the question is, which target is the best? All agree that it's too early to tell.
Such is the hardware for deep brain stimulation -- the equivalent of a cardiac pacemaker for the mind.
Until recently, deep brain stimulation was approved in the U.S. only to treat certain movement disorders, primarily those of Parkinson's disease, for which it diminishes tremors and rigidity and improves mobility. To date, more than 60,000 patients worldwide have had the devices implanted.
But now use of the technique seems set to mushroom.
This year, the Food and Drug Administration granted a so-called humanitarian device exemption for the treatment to be used in severe cases of obsessive-compulsive disorder -- the first approval of deep brain stimulation therapy for any psychiatric condition.
Large clinical trials are also in the works for use of deep brain stimulation for epilepsy and depression, and experimental studies in the U.S. and elsewhere -- still in their early stages -- are exploring the treatment for obesity, traumatic brain injury, severe chronic pain, Alzheimer's disease, anorexia, tinnitus and addiction.
There are discussions too on the possible use of deep brain stimulation to treat hypertension.
"The field is taking off," says Dr. Ali Rezai, director of functional neurosurgery at the Cleveland Clinic, who has been involved in research on movement disorders, traumatic brain injury, obsessive-compulsive disorder and severe depression, among others.
Some researchers warn, however, that with all this activity -- pushed in part by the industry that makes the brain-stimulation devices -- the field may be moving too fast.
"There is so much progress that's been made and so much potential -- you would hate to lose that potential," says Dr. Joseph Fins, chief of the division of medical ethics and a professor at Weill Cornell Medical College in New York.
Here's a look at deep brain stimulation as it moves beyond Parkinson's disease. (See the related story about reservations scientists have about the growth of the field, and go online at latimes.com/health for a look at less-explored applications such as traumatic brain injury and obesity.)
Obsessive- compulsive disorder
In studies with a total of 26 patients with severe obsessive-compulsive disorder, 60% of those whose device was turned on demonstrated "very much improved" symptoms after months of deep brain stimulation as measured by interviews and questionnaires, says Dr. Benjamin Greenberg, an associate professor at Brown University Medical School and Butler Hospital in Providence, R.I., who was one of the study researchers.
The patients had previously failed on medicines as well as behavioral cognitive therapy.
Yet the data, published last year in Molecular Psychiatry, can't really nail the effect of the treatment, Greenberg says, because the patients for the most part knew whether their devices were turned on or off. Thus, researchers can't rule out that some of the observed improvements were due to a placebo effect.
Patients were stimulated in an area called ventral capsule/ventral striatum, chosen, in part, because removal of nerve fibers in that area is known to cause improvement in obsessive-compulsive symptoms.
Based largely on these findings, the FDA recently granted a limited humanitarian device exemption that permits the device to be used in as many as 4,000 of the country's most severe cases of obsessive compulsive disorder per year.
To get this kind of exemption, Medtronic -- makers of the only deep brain stimulation device that is FDA-approved -- needed only to show its safety and probable benefit.
Greenberg is now doing a randomized, double-blinded trial with 30 patients, some of whom have devices turned on right away and some who have them turned on after a delay. No one will know whose device is turned on for the first several months of the trial.
Medtronic has conducted a large-scale randomized trial for deep brain stimulation on epilepsy. Data will be submitted to the FDA this year, says Paul Stypulkowski, senior director of therapy research of Medtronic.
The device was turned on, for three months, in half of the 110 volunteers, stimulating -- and thereby, paradoxically, inhibiting-- an area called the anterior nucleus of the thalamus. That area is believed to influence a circuit involved in seizures.
The data, presented in December at a meeting in Seattle, show that deep brain stimulation reduced the number of seizures by 38% compared with what was seen before implanting the device.
That is slightly better than improvement seen with vagus nerve stimulation, another FDA-approved electrical stimulation treatment, which reduces seizures by about 25%.
The control group whose device was kept turned off, also improved, by 14.5%. That could be due to a placebo effect. Or it might be because people who join trials are usually at their worst -- and often tend to improve somewhat on their own, says trial researcher Dr. Douglas Labar, of the Weill Cornell Medical College in New York.
If deep brain stimulation is approved, Labar says, patients will have the choice between a more efficient but also more risky treatment and the slightly less efficient but also less risky vagus nerve stimulation.
Depression
Medtronic and a second company, St. Paul, Minn.-based St. Jude Medical, have two large-scale randomized trials underway for severe, treatment-resistant depression. (St. Jude Medical recently received approval to sell its device for the treatment of Parkinson's disease in Europe and is now completing studies aimed at securing FDA approval for treating Parkinson's and another movement disorder in the U.S.)
Medtronic's depression trial will follow about 200 patients stimulated in an area called the anterior limb of the internal capsule for at least one year.
This brain target for depression was identified by accident: When obsessive-compulsive disorder patients who also had depression were stimulated in this area, their depression also improved.
In one case, a patient produced a one-sided smile when stimulated on one side of the brain and also expressed feelings of happiness, says study researcher Dr. Wayne Goodman of the National Institute of Mental Health.
In a recently published unblinded study, about half of 15 patients showed at least a 50% improvement in severe depression symptoms a year or more after surgery when the anterior limb of the internal capsule was stimulated, says Rezai, who was involved in the study.
St. Jude Medical chose a different brain target, area 25, for its depression trial, which will enroll more than 100 patients. Brain imaging studies have shown that area 25 is more active in depressed people.
In a study of 20 patients, 55% still responded to treatment as late as one year after surgery, says study author Dr. Helen Mayberg, professor of psychiatry and neurology at Emory University. That is an "unheard-of response rate" given that these patients had tried and failed every other treatment, including several medications and electroconvulsive therapy, Mayberg says.
By comparison, Mayberg says, stimulation of the vagus nerve in the neck, approved by the FDA for depression, has only a 15% response rate at 10 weeks in similarly severely depressed patients.
Dr. Thomas Schlaepfer, vice chairman of the department of psychiatry of the University of Bonn in Germany, has been treating severely depressed patients by stimulating yet a third brain target, the nucleus accumbens.
The nucleus accumbens doesn't show normal activity in depressed patients, which could explain why they are less able to experience pleasure.
Last year, Schlaepfer showed that deep brain stimulation in this area led to acute improvements in three severely depressed patients. He says he has extended the work to 10 patients, half of whom showed an improvement when examined a year later.
With deep brain stimulation now being tried in at least three brain areas for depression, the question is, which target is the best? All agree that it's too early to tell.
Sunday, May 10, 2009
Mayo Clinic Study Finds Anemia Might be Associated With Development of Parkinson's Disease
Mayo Clinic Study Finds Anemia Might be Associated With Development of Parkinson's Disease
ROCHESTER, Minn. — Results of a new Mayo Clinic study support an association between anemia experienced early in life and the development of Parkinson's disease many years later. The findings will be presented at the American Academy of Neurology Annual Meeting in Seattle on April 30, 2009.
"We were surprised to discover that chronic anemia or low levels of hemoglobin were linked to the risk of Parkinson's disease 20-30 years later," says Walter Rocca, M.D. an author of the study and a neurologist at Mayo Clinic.
Hemoglobin is the protein that transports oxygen in the blood, an essential element for life. "We looked at both anemia as diagnosed by a physician and low hemoglobin values," Dr. Rocca says. "Both were associated with an increased risk of Parkinson's disease. This might indicate that Parkinson's disease actually starts 20--30 years before we see any motor changes in the body."
The case-control study included 196 people who developed Parkinson's disease in Olmsted County, Minn., from 1976 through 1995. Each case was matched by age and sex to a general population control subject who was not affected by Parkinson's disease. The medical records of cases and controls were reviewed using the resources of the Rochester Epidemiology Project to determine if there was a link between anemia or low hemoglobin levels and the risk of developing Parkinson's disease many years later. Anemia was significantly more common in the history of cases than in the history of controls.
Dr. Rocca and his team hope to replicate these results in another population group. "We first need to confirm the study results. If the findings are replicated, we will try to understand what are the underlying mechanisms. Understanding the mechanisms may lead to new ways to prevent or treat Parkinson's disease," Dr. Rocca says.
Other members of the Mayo Clinic research team included Rodolfo Savica, M.D.; Justin Carlin; Brandon Grossardt; James Bower, M.D.; and Demetrius Maraganore, M.D.
ROCHESTER, Minn. — Results of a new Mayo Clinic study support an association between anemia experienced early in life and the development of Parkinson's disease many years later. The findings will be presented at the American Academy of Neurology Annual Meeting in Seattle on April 30, 2009.
"We were surprised to discover that chronic anemia or low levels of hemoglobin were linked to the risk of Parkinson's disease 20-30 years later," says Walter Rocca, M.D. an author of the study and a neurologist at Mayo Clinic.
Hemoglobin is the protein that transports oxygen in the blood, an essential element for life. "We looked at both anemia as diagnosed by a physician and low hemoglobin values," Dr. Rocca says. "Both were associated with an increased risk of Parkinson's disease. This might indicate that Parkinson's disease actually starts 20--30 years before we see any motor changes in the body."
The case-control study included 196 people who developed Parkinson's disease in Olmsted County, Minn., from 1976 through 1995. Each case was matched by age and sex to a general population control subject who was not affected by Parkinson's disease. The medical records of cases and controls were reviewed using the resources of the Rochester Epidemiology Project to determine if there was a link between anemia or low hemoglobin levels and the risk of developing Parkinson's disease many years later. Anemia was significantly more common in the history of cases than in the history of controls.
Dr. Rocca and his team hope to replicate these results in another population group. "We first need to confirm the study results. If the findings are replicated, we will try to understand what are the underlying mechanisms. Understanding the mechanisms may lead to new ways to prevent or treat Parkinson's disease," Dr. Rocca says.
Other members of the Mayo Clinic research team included Rodolfo Savica, M.D.; Justin Carlin; Brandon Grossardt; James Bower, M.D.; and Demetrius Maraganore, M.D.
Saturday, May 2, 2009
Parkinson's Disease: More Than Shaking Going On Researchers discovering non-motor symptoms may happen first
Parkinson's Disease: More Than Shaking Going On Researchers discovering non-motor symptoms may happen first
(live-PR.com) - TORONTO, ONTARIO -- (Marketwire) -- 04/21/09 -- Parkinson's is much more than a tremor. That's a message Parkinson Society Canada hopes to drive home this April during Parkinson's Awareness Month.
In Parkinson's, the most common symptoms are movement-related: tremor, slowness, muscle stiffness and balance problems. However, by the time Parkinson's is diagnosed, people have already lost 60 to 70 percent of the dopamine-producing cells. Now researchers are discovering that non-motor symptoms such as sleep problems, depression and smell loss may represent the earliest signs of Parkinson's, for some people, and may appear years before the diagnosis.
In research at Montreal's Sacre-Coeur Hospital, Dr. Ronald Postuma, assistant professor of neurology at McGill University found that people with a rare sleep disorder where they physically acted out their dreams had a 50% risk of developing Parkinson's disease or dementia within 12 years. The patients had REM-sleep behaviour disorder, which Postuma describes as "punching and yelling or kicking out while asleep. It mostly affects people in their 60s and 70s, almost always men." Not all will develop a neurodegenerative disease but Postuma says, "Patients with true REM-sleep behaviour disorder have a considerable risk of developing Parkinson's disease."
Depression and anxiety can surface early in Parkinson's. "Many people, as they're starting to lose their dopamine, may not yet have developed a tremor, slowness or trouble walking, but may feel anxious and depressed," says Dr. Susan Fox, assistant professor of neurology at University of Toronto. "Depression is also part of Parkinson's disease itself and not just a reaction to having a chronic neurological disorder." Fox notes untreated depression can reduce quality of life.
Smell loss is a common occurrence. "The general consensus is that the changes in olfaction (sense of smell) occur about five years before the Parkinson's diagnosis." says Dr. Harold Robertson, a professor in the Brain Repair Centre and Department of Pharmacology at Dalhousie University in Halifax. "That could give us enough lead time to try to stop the process."
Joyce Gordon, Parkinson Society Canada President and CEO says "The more dollars we can put towards Parkinson's research, the sooner we may be able to establish if there is a definite link to Parkinson's when a person has sleep problems, depression or loss of smell. This would lay the groundwork for developing treatments to delay or stop this debilitating disease in its tracks. The answers can't come soon enough for the 100,000 Canadians who have Parkinson's disease and those who are unknowingly at risk."
In the meantime, the first step for anyone experiencing difficulties with sleep or mood is to see a doctor for a proper diagnosis. REM sleep behaviour disorder and depression are treatable. Smell loss is not currently treatable but is worth mentioning to the doctor, during a routine visit, as it may be due to a variety of causes.
Parkinson's is a progressive neurological disease for which there is no known cause or cure. When cells in the brain that normally produce a chemical called "dopamine" die, symptoms of Parkinson's appear. The most common symptoms are: tremor (shaking), slowness in movements, muscle stiffness and problems with balance. Other symptoms that may also occur for some people include fatigue, difficulties with speech and writing, sleep disorders, depression and cognitive changes.
For over 40 years, Parkinson Society Canada (PSC) has been the national voice of people living with Parkinson's disease. PSC has over 230 chapters and support groups. PSC's mission is to fund research, support services, advocacy and education.
For more information on Parkinson's disease and Parkinson Society Canada, visit the PSC website at www.parkinson.ca : www.parkinson.ca or call 1-800-565-3000.
Contacts:
Parkinson Society Canada
John Provenzano
416-227-3399 or 1-800-565-3000 ext 3399
John.provenzano@parkinson.ca : John.provenzano@parkinson.ca
(live-PR.com) - TORONTO, ONTARIO -- (Marketwire) -- 04/21/09 -- Parkinson's is much more than a tremor. That's a message Parkinson Society Canada hopes to drive home this April during Parkinson's Awareness Month.
In Parkinson's, the most common symptoms are movement-related: tremor, slowness, muscle stiffness and balance problems. However, by the time Parkinson's is diagnosed, people have already lost 60 to 70 percent of the dopamine-producing cells. Now researchers are discovering that non-motor symptoms such as sleep problems, depression and smell loss may represent the earliest signs of Parkinson's, for some people, and may appear years before the diagnosis.
In research at Montreal's Sacre-Coeur Hospital, Dr. Ronald Postuma, assistant professor of neurology at McGill University found that people with a rare sleep disorder where they physically acted out their dreams had a 50% risk of developing Parkinson's disease or dementia within 12 years. The patients had REM-sleep behaviour disorder, which Postuma describes as "punching and yelling or kicking out while asleep. It mostly affects people in their 60s and 70s, almost always men." Not all will develop a neurodegenerative disease but Postuma says, "Patients with true REM-sleep behaviour disorder have a considerable risk of developing Parkinson's disease."
Depression and anxiety can surface early in Parkinson's. "Many people, as they're starting to lose their dopamine, may not yet have developed a tremor, slowness or trouble walking, but may feel anxious and depressed," says Dr. Susan Fox, assistant professor of neurology at University of Toronto. "Depression is also part of Parkinson's disease itself and not just a reaction to having a chronic neurological disorder." Fox notes untreated depression can reduce quality of life.
Smell loss is a common occurrence. "The general consensus is that the changes in olfaction (sense of smell) occur about five years before the Parkinson's diagnosis." says Dr. Harold Robertson, a professor in the Brain Repair Centre and Department of Pharmacology at Dalhousie University in Halifax. "That could give us enough lead time to try to stop the process."
Joyce Gordon, Parkinson Society Canada President and CEO says "The more dollars we can put towards Parkinson's research, the sooner we may be able to establish if there is a definite link to Parkinson's when a person has sleep problems, depression or loss of smell. This would lay the groundwork for developing treatments to delay or stop this debilitating disease in its tracks. The answers can't come soon enough for the 100,000 Canadians who have Parkinson's disease and those who are unknowingly at risk."
In the meantime, the first step for anyone experiencing difficulties with sleep or mood is to see a doctor for a proper diagnosis. REM sleep behaviour disorder and depression are treatable. Smell loss is not currently treatable but is worth mentioning to the doctor, during a routine visit, as it may be due to a variety of causes.
Parkinson's is a progressive neurological disease for which there is no known cause or cure. When cells in the brain that normally produce a chemical called "dopamine" die, symptoms of Parkinson's appear. The most common symptoms are: tremor (shaking), slowness in movements, muscle stiffness and problems with balance. Other symptoms that may also occur for some people include fatigue, difficulties with speech and writing, sleep disorders, depression and cognitive changes.
For over 40 years, Parkinson Society Canada (PSC) has been the national voice of people living with Parkinson's disease. PSC has over 230 chapters and support groups. PSC's mission is to fund research, support services, advocacy and education.
For more information on Parkinson's disease and Parkinson Society Canada, visit the PSC website at www.parkinson.ca : www.parkinson.ca or call 1-800-565-3000.
Contacts:
Parkinson Society Canada
John Provenzano
416-227-3399 or 1-800-565-3000 ext 3399
John.provenzano@parkinson.ca : John.provenzano@parkinson.ca
Sunday, April 26, 2009
Studies Show 3 out of 4 Parkinson's Disease Patients Can Improve Walking and Quality of Life Within 2 Weeks
Studies Show 3 out of 4 Parkinson's Disease Patients Can Improve Walking and Quality of Life Within 2 Weeks
Newly released virtual reality gait training device shown to improve quality of life for Parkinson's disease and other movement disorders.
Haifa, Israel (PRWEB) April 13, 2009 -- Parkinson's disease patients are discovering first-hand that daily exercise with a new virtual reality device, the GaitAid, has a positive effect on their walking ability, minimizing balance problems and freezing, and improving quality of life. The GaitAid offers a drug free, non RX alternative with no side effects.
As soon as I tried it my mobility improved tremendously! For the first time in over a year I am already walking without a cane. I am so impressed and so grateful. I was dreading my planned trip out of the country until I received your glasses. I cannot wait to share the miracle with my friends who suffer from PD. Thank you!
Gait velocity and stride length were improved in PD patients after training with a visual-and-auditory virtual cueing system, with a marked residual effect. Devices utilizing closed-loop visual feedback system are desirable non-pharmacologic interventions to improve walking in PD.
Daniel Neal, a Parkinson's disease patient from Palm Springs, CA., commented after receiving his GaitAid, "As soon as I tried it my mobility improved tremendously! For the first time in over a year I am already walking without a cane. I am so impressed and so grateful. I was dreading my planned trip out of the country until I received your glasses. I cannot wait to share the miracle with my friends who suffer from PD. Thank you!"
Yoram Baram, a computer science professor and incumbent of the Roy Matas / Winnipeg Chair in Biomedical Engineering at the Technion, Israel Institute of Technology has collaborated with several neurologists specializing in treating Parkinson's disease, Multiple Sclerosis and other movement disorders, in developing and testing a new, non-invasive training device designed to proactively minimize freezing and balance problems during walking. The noticeable physical and mental improvement of patients participating in clinical studies led Baram to bring the GaitAid device to market as a FDA registered medical device and is offering the device for a no risk trial period on his company's website (www.medigait.com).
Alberto J. Espay, MD, from the Neuroscience Institute, Department of Neurology, Movement Disorders Center, University of Cincinnati, specializes in research and clinical treatment of movement disorders. After offering the GaitAid to a group of his Parkinson's disease patients to use at home, Dr. Espay states, "Gait velocity and stride length were improved in PD patients after training with a visual-and-auditory virtual cueing system, with a marked residual effect. Devices utilizing closed-loop visual feedback system are desirable non-pharmacologic interventions to improve walking in PD."
The easy to use device includes special glasses and earphones which provide sensory feedback in response to the patient's movements. A practice session involves walking with the device for up to twenty minutes with no special training needed. These practice sessions soon start to evoke a lasting improvement for most Parkinson's disease patients. The degree of improvement varies, some patients use the GaitAid only occasionally after a few months while others make a short session a part of their daily routine to keep their results.
Parkinson's disease remains a mystery of medical science. For reason's unknown, certain brain cells stop producing a substance called Dopamine, which affects an individual's movement, strength and balance. There is currently no cure, though stem cell research offers future promise.
Emerging scientific evidence confirms that movement lessens neurological deterioration that contributes to Parkinson's Disease progression.
The device is available for a no risk trial period of 60 days:
online www.medigait.com
email: support (at) medigait (dot) com
or by phone 888-777-9906.
Newly released virtual reality gait training device shown to improve quality of life for Parkinson's disease and other movement disorders.
Haifa, Israel (PRWEB) April 13, 2009 -- Parkinson's disease patients are discovering first-hand that daily exercise with a new virtual reality device, the GaitAid, has a positive effect on their walking ability, minimizing balance problems and freezing, and improving quality of life. The GaitAid offers a drug free, non RX alternative with no side effects.
As soon as I tried it my mobility improved tremendously! For the first time in over a year I am already walking without a cane. I am so impressed and so grateful. I was dreading my planned trip out of the country until I received your glasses. I cannot wait to share the miracle with my friends who suffer from PD. Thank you!
Gait velocity and stride length were improved in PD patients after training with a visual-and-auditory virtual cueing system, with a marked residual effect. Devices utilizing closed-loop visual feedback system are desirable non-pharmacologic interventions to improve walking in PD.
Daniel Neal, a Parkinson's disease patient from Palm Springs, CA., commented after receiving his GaitAid, "As soon as I tried it my mobility improved tremendously! For the first time in over a year I am already walking without a cane. I am so impressed and so grateful. I was dreading my planned trip out of the country until I received your glasses. I cannot wait to share the miracle with my friends who suffer from PD. Thank you!"
Yoram Baram, a computer science professor and incumbent of the Roy Matas / Winnipeg Chair in Biomedical Engineering at the Technion, Israel Institute of Technology has collaborated with several neurologists specializing in treating Parkinson's disease, Multiple Sclerosis and other movement disorders, in developing and testing a new, non-invasive training device designed to proactively minimize freezing and balance problems during walking. The noticeable physical and mental improvement of patients participating in clinical studies led Baram to bring the GaitAid device to market as a FDA registered medical device and is offering the device for a no risk trial period on his company's website (www.medigait.com).
Alberto J. Espay, MD, from the Neuroscience Institute, Department of Neurology, Movement Disorders Center, University of Cincinnati, specializes in research and clinical treatment of movement disorders. After offering the GaitAid to a group of his Parkinson's disease patients to use at home, Dr. Espay states, "Gait velocity and stride length were improved in PD patients after training with a visual-and-auditory virtual cueing system, with a marked residual effect. Devices utilizing closed-loop visual feedback system are desirable non-pharmacologic interventions to improve walking in PD."
The easy to use device includes special glasses and earphones which provide sensory feedback in response to the patient's movements. A practice session involves walking with the device for up to twenty minutes with no special training needed. These practice sessions soon start to evoke a lasting improvement for most Parkinson's disease patients. The degree of improvement varies, some patients use the GaitAid only occasionally after a few months while others make a short session a part of their daily routine to keep their results.
Parkinson's disease remains a mystery of medical science. For reason's unknown, certain brain cells stop producing a substance called Dopamine, which affects an individual's movement, strength and balance. There is currently no cure, though stem cell research offers future promise.
Emerging scientific evidence confirms that movement lessens neurological deterioration that contributes to Parkinson's Disease progression.
The device is available for a no risk trial period of 60 days:
online www.medigait.com
email: support (at) medigait (dot) com
or by phone 888-777-9906.
Sunday, April 19, 2009
Shedding some light on Parkinson's treatment
Shedding some light on Parkinson's treatment
EUREKALERT
Contact: Lisa Van Pay
lvanpay@nsf.gov
703-292-8796
National Science Foundation
Scientists use optical approach to study deep brain stimulation
A research team lead by Karl Deisseroth in the bioengineering department at Stanford University has developed a technique to systematically characterize disease circuits in the brain. By precisely controlling individual components of the circuit implicated in Parkinson's disease, the team has identified a specific group of cells as direct targets of deep brain stimulation (DBS), a Parkinson's treatment.
Termed optogenetics, the NSF-funded technology uses light-activated proteins, originally isolated from bacteria, in combination with genetic approaches to control specific parts of the brain. The technique is a vast improvement over previous methods because it allows researchers to precisely stimulate neurons and measure the effect of treatment simultaneously in animals with Parkinson's-like symptoms.
Published in the April 17 issue of Science, Deisseroth's team found they could reduce disease symptoms by preferentially activating neurons that link to the subthalamic nucleus region of the brain. First, these specific cells were treated in a way that made them sensitive to stimulation by blue light, then the team implanted an optical fiber in the brain.
When researchers rapidly flashed blue light inside the animals' brains the disease symptoms improved. In contrast, treating with slower flashes of light actually made the symptoms worse, and targeting other kinds of cells had no effect at all, indicating both proper cell type and stimulation frequency are crucial components of effective treatment. Flashing blue light on portions of the same neurons found closer to the outer surface of the brain had an effect similar to treatment deep within the brain, raising the possibility that researchers may be able to develop treatments that are less invasive than current options.
Approved as a medical treatment in 1997, DBS remains controversial because it doesn't work on all patients. Used to treat Parkinson's disease, depression and movement disorders, DBS involves surgical implantation of a brain pacemaker, which sends electrical impulses into the brain. In the past, researchers have been unable to understand the effective mechanism of DBS because the electrical signal emitted by DBS devices interferes with the ability to observe brain activity.
Explains Deisseroth, "The brain is an electrical device, but it is a very complicated device. Think of it as an orchestra without sections: all of the types of instruments, or cells, are mixed together. Treatments like DBS are unrefined, in that they stimulate all of the cells or instruments. The optogenetic approach allows us to control stimulation of specific cells in the brain on the appropriate timescale, much like a conductor directing specific sections of an orchestra at the appropriate time."
Production of new therapies is always a long-term goal, but for now Deisseroth and his group are focused on mapping disease circuits and understanding brain function. "We need to understand the players before we can develop effective treatment strategies," he stated.
EUREKALERT
Contact: Lisa Van Pay
lvanpay@nsf.gov
703-292-8796
National Science Foundation
Scientists use optical approach to study deep brain stimulation
A research team lead by Karl Deisseroth in the bioengineering department at Stanford University has developed a technique to systematically characterize disease circuits in the brain. By precisely controlling individual components of the circuit implicated in Parkinson's disease, the team has identified a specific group of cells as direct targets of deep brain stimulation (DBS), a Parkinson's treatment.
Termed optogenetics, the NSF-funded technology uses light-activated proteins, originally isolated from bacteria, in combination with genetic approaches to control specific parts of the brain. The technique is a vast improvement over previous methods because it allows researchers to precisely stimulate neurons and measure the effect of treatment simultaneously in animals with Parkinson's-like symptoms.
Published in the April 17 issue of Science, Deisseroth's team found they could reduce disease symptoms by preferentially activating neurons that link to the subthalamic nucleus region of the brain. First, these specific cells were treated in a way that made them sensitive to stimulation by blue light, then the team implanted an optical fiber in the brain.
When researchers rapidly flashed blue light inside the animals' brains the disease symptoms improved. In contrast, treating with slower flashes of light actually made the symptoms worse, and targeting other kinds of cells had no effect at all, indicating both proper cell type and stimulation frequency are crucial components of effective treatment. Flashing blue light on portions of the same neurons found closer to the outer surface of the brain had an effect similar to treatment deep within the brain, raising the possibility that researchers may be able to develop treatments that are less invasive than current options.
Approved as a medical treatment in 1997, DBS remains controversial because it doesn't work on all patients. Used to treat Parkinson's disease, depression and movement disorders, DBS involves surgical implantation of a brain pacemaker, which sends electrical impulses into the brain. In the past, researchers have been unable to understand the effective mechanism of DBS because the electrical signal emitted by DBS devices interferes with the ability to observe brain activity.
Explains Deisseroth, "The brain is an electrical device, but it is a very complicated device. Think of it as an orchestra without sections: all of the types of instruments, or cells, are mixed together. Treatments like DBS are unrefined, in that they stimulate all of the cells or instruments. The optogenetic approach allows us to control stimulation of specific cells in the brain on the appropriate timescale, much like a conductor directing specific sections of an orchestra at the appropriate time."
Production of new therapies is always a long-term goal, but for now Deisseroth and his group are focused on mapping disease circuits and understanding brain function. "We need to understand the players before we can develop effective treatment strategies," he stated.
Sunday, April 12, 2009
Arrayit Corporation and The Parkinson's Institute Announce New Research Collaboration
Arrayit Corporation and The Parkinson's Institute Announce New Research Collaboration
ARYC 2.63, -0.37, -12.5%) , a proprietary life sciences technology leader, announces a new research collaboration with The Parkinson's Institute of Sunnyvale, California to discover biomarkers for Parkinson's disease. This unique study involves the prospective collection of samples from well-characterized Parkinson's patients combined with Arrayit's new H25K microarray technology. The first experiments have enabled rapid and efficient sample preparation of specimens from Parkinson's disease patients, an important step in the discovery of molecular markers for Parkinson's disease.
"This collaboration provides an important first step towards unraveling the mysteries of Parkinson's disease," stated Dr. Mark Schena, Ph.D., Arrayit President. "We look forward to working with The Parkinson's Institute to decipher the molecular basis of the disease," he continued. The Parkinson's Institute Assistant Professor Dr. Birgitt Schuele, M.D. added, "Parkinson's disease represents a serious and challenging medical condition. We are pleased to be deploying Arrayit technology to combat this illness."
About Arrayit Corporation
Arrayit Corporation, headquartered in Sunnyvale, California, leads and empowers the genetic, research, pharmaceutical, and diagnostic communities through the discovery, development and manufacture of proprietary life science technologies and consumables for disease prevention, treatment and cure. It now offers over 650 products to a customer base of more than 2,500 laboratories worldwide, including most every major university, pharmaceutical and biotech company, major agricultural and chemical company, government agency, national research foundation and many private sector enterprises. Please visit www.arrayit.com for more information.
About The Parkinson's Institute
The Parkinson's Institute and Clinical Center (PI) is America's only independent non-profit organization that provides basic and clinical research, clinical trials and a comprehensive movement disorder patient clinic for Parkinson's disease (PD) and related neurological movement disorders, all under one roof. Our mission is to find the causes, provide first class patient care and discover a cure. Our unique freestanding organization supports a strong collaboration of translational medicine designed to more directly connect research to patient care -- from the "bench to bedside." Please visit www.thepi.org for more information.
Safe Harbor Statement
Except for historical information contained herein, statements made in this release that would constitute forward-looking statements may involve certain risks and uncertainties. All forward-looking statements made in this release are based on currently available information and the Company assumes no responsibility to update any such forward-looking statement. The following factors, among others, may cause actual results to differ materially from the results suggested in the forward-looking statements. The factors include, but are not limited to, risks that may result from changes in the Company's business operations; our ability to keep pace with technological advances; significant competition in the biomedical business; our relationships with key suppliers and customers; quality and consumer acceptance of newly introduced products; market volatility; non-availability of product; excess inventory; price and product competition; new product introductions, the outcome of our legal disputes; the possibility that the review of our prior filings by the SEC may result in changes to our financial statements; and the possibility that stockholders or regulatory authorities may initiate proceedings against Arrayit and/or our officers and directors as a result of any restatements. Risk factors associated with our business, including some of the facts set forth herein, are detailed in the Company's Form 10-K for the fiscal year ended December 31, 2007 and Form 10-Q/A for the fiscal first quarter ended March 31, 2008 and Form 10-Q for the fiscal second quarter ended June 30, 2008.
ARYC 2.63, -0.37, -12.5%) , a proprietary life sciences technology leader, announces a new research collaboration with The Parkinson's Institute of Sunnyvale, California to discover biomarkers for Parkinson's disease. This unique study involves the prospective collection of samples from well-characterized Parkinson's patients combined with Arrayit's new H25K microarray technology. The first experiments have enabled rapid and efficient sample preparation of specimens from Parkinson's disease patients, an important step in the discovery of molecular markers for Parkinson's disease.
"This collaboration provides an important first step towards unraveling the mysteries of Parkinson's disease," stated Dr. Mark Schena, Ph.D., Arrayit President. "We look forward to working with The Parkinson's Institute to decipher the molecular basis of the disease," he continued. The Parkinson's Institute Assistant Professor Dr. Birgitt Schuele, M.D. added, "Parkinson's disease represents a serious and challenging medical condition. We are pleased to be deploying Arrayit technology to combat this illness."
About Arrayit Corporation
Arrayit Corporation, headquartered in Sunnyvale, California, leads and empowers the genetic, research, pharmaceutical, and diagnostic communities through the discovery, development and manufacture of proprietary life science technologies and consumables for disease prevention, treatment and cure. It now offers over 650 products to a customer base of more than 2,500 laboratories worldwide, including most every major university, pharmaceutical and biotech company, major agricultural and chemical company, government agency, national research foundation and many private sector enterprises. Please visit www.arrayit.com for more information.
About The Parkinson's Institute
The Parkinson's Institute and Clinical Center (PI) is America's only independent non-profit organization that provides basic and clinical research, clinical trials and a comprehensive movement disorder patient clinic for Parkinson's disease (PD) and related neurological movement disorders, all under one roof. Our mission is to find the causes, provide first class patient care and discover a cure. Our unique freestanding organization supports a strong collaboration of translational medicine designed to more directly connect research to patient care -- from the "bench to bedside." Please visit www.thepi.org for more information.
Safe Harbor Statement
Except for historical information contained herein, statements made in this release that would constitute forward-looking statements may involve certain risks and uncertainties. All forward-looking statements made in this release are based on currently available information and the Company assumes no responsibility to update any such forward-looking statement. The following factors, among others, may cause actual results to differ materially from the results suggested in the forward-looking statements. The factors include, but are not limited to, risks that may result from changes in the Company's business operations; our ability to keep pace with technological advances; significant competition in the biomedical business; our relationships with key suppliers and customers; quality and consumer acceptance of newly introduced products; market volatility; non-availability of product; excess inventory; price and product competition; new product introductions, the outcome of our legal disputes; the possibility that the review of our prior filings by the SEC may result in changes to our financial statements; and the possibility that stockholders or regulatory authorities may initiate proceedings against Arrayit and/or our officers and directors as a result of any restatements. Risk factors associated with our business, including some of the facts set forth herein, are detailed in the Company's Form 10-K for the fiscal year ended December 31, 2007 and Form 10-Q/A for the fiscal first quarter ended March 31, 2008 and Form 10-Q for the fiscal second quarter ended June 30, 2008.
Sunday, April 5, 2009
Parkinson's Stem Cell Implants Yield Nightmarish Side Effects
Parkinson's Stem Cell Implants Yield Nightmarish Side Effects
Gina Kolata/ NY Times
A study that attempted to treat Parkinson's disease by implanting cells from aborted fetuses into patients' brains not only failed to show an overall benefit but also revealed a disastrous side effect, scientists report.
In about 15% of patients, the cells apparently grew too well, churning out so much of a chemical that controls movement that the patients writhed and jerked uncontrollably. The researchers say there is no way to remove or deactivate the transplanted cells.
On their advice the six patients who enrolled in the study but who had not yet had the operation have decided to forego it.
The results, reported in the New England Journal of Medicine, are a severe blow to what had been considered a highly promising avenue of research for treating Parkinson's disease, Alzheimer's disease and other neurological ailments.
The study indicates that the simple solution of injecting fetal brain cells into a patient's brain may not be enough to treat complex diseases involving nerve cells and connections that are poorly understood.
Some say it is time to go back to the laboratory and to animals before doing any more operations on humans. The findings also may fuel the debate over whether it is appropriate to use fetal tissue from aborted fetuses to treat diseases.
Despite their disappointment, some researchers said they hoped that the results would not bring fetal cell research to a grinding halt. The research has been controversial because the fetal cells were obtained from abortion clinics.
"This is still our one great hope for a cure," said J. William Langston, who is scientific director and chief executive officer at The Parkinson's Institute in Sunnyvale, CA.
Parkinson's disease occurs when for unknown reasons, cells of the substantia nigra in the base of the brain die. The hope was that fetal substantia nigra cells might take over for them. But the study showed in older patients, the operation had no benefit and in some younger patients, the transplants brought on nightmarish effects.
Although the paper depicts the patients with side effect in impassive clinical terms, doctors who have seen them paint a much different picture. Paul. E. Greene, a neurologist at Columbia University's College of Physicians and Surgeons and a researcher in the study, said the uncontrollable movements some patients suffer are "absolutely devastating."
"They chew constantly, their fingers go up and down, their wrists flex and distend," he said. And the patients writhe and twist, jerk their heads, fling their arms about."It was tragic, catastrophic," Greene said. "It's a real nightmare. And we can't selectively turn it off."
One man was so badly affected that he could no longer eat and had to use a feeding tube, Greene said. In another, the condition came and went unpredictably throughout the day, and when it occurred, the man's speech was unintelligible.
For now, Greene said, his position is clear: "No more fetal transplants. We are absolutely and adamantly convinced that this should be considered for research only. And whether it should be research in people is an open question."
Gerard D. Fischbach, who was director of the National Institutes of Neurological Disorders and Stroke, which sponsored the study and is now dean of the faculty of medicine at Columbia University's College of Physicians and Surgeons said that while the operation had been promoted by some neurosurgeons as miraculous, this was the first time it was rigorously evaluated, using sham surgery as a comparison. Fischbach was the director of the institute only at the end of the study.
"Ad hoc reports of spectacular results can always occur," Fischbach said. "But if you do these studies systematically, this is the result you get."
In the study, researchers led by Curt R. Freed of the University of Colorado Health Sciences Center in Denver and Stanley Fahn of Columbia University's College of Physicians and Surgeons, recruited 40 patients, aged 34 to 75, who had Parkinson's disease for an average of 14 years. The patients were randomly assigned to have substantia nigra cells from four fetuses implanted in their brains or to have sham surgery for comparison.
The surgery took place in Colorado and the patients were evaluated in New York. The fetal cell surgery involved drilling four small holes in the patient's forehead and then inserting long needles through the holes into the brain and injecting the fetal cells. The sham surgery involved drilling the holes but not injecting needles into the brain.
The study's primary measure of success was whether the patients themselves noticed that they were better, as determined by a survey that they mailed in a year later but before they knew whether they had fetal cell implants or not. The study found no difference between the two groups - neither those who had the fetal cell operation nor those who had the sham surgery noticed an improvement in their symptoms.
__________________
Gina Kolata/ NY Times
A study that attempted to treat Parkinson's disease by implanting cells from aborted fetuses into patients' brains not only failed to show an overall benefit but also revealed a disastrous side effect, scientists report.
In about 15% of patients, the cells apparently grew too well, churning out so much of a chemical that controls movement that the patients writhed and jerked uncontrollably. The researchers say there is no way to remove or deactivate the transplanted cells.
On their advice the six patients who enrolled in the study but who had not yet had the operation have decided to forego it.
The results, reported in the New England Journal of Medicine, are a severe blow to what had been considered a highly promising avenue of research for treating Parkinson's disease, Alzheimer's disease and other neurological ailments.
The study indicates that the simple solution of injecting fetal brain cells into a patient's brain may not be enough to treat complex diseases involving nerve cells and connections that are poorly understood.
Some say it is time to go back to the laboratory and to animals before doing any more operations on humans. The findings also may fuel the debate over whether it is appropriate to use fetal tissue from aborted fetuses to treat diseases.
Despite their disappointment, some researchers said they hoped that the results would not bring fetal cell research to a grinding halt. The research has been controversial because the fetal cells were obtained from abortion clinics.
"This is still our one great hope for a cure," said J. William Langston, who is scientific director and chief executive officer at The Parkinson's Institute in Sunnyvale, CA.
Parkinson's disease occurs when for unknown reasons, cells of the substantia nigra in the base of the brain die. The hope was that fetal substantia nigra cells might take over for them. But the study showed in older patients, the operation had no benefit and in some younger patients, the transplants brought on nightmarish effects.
Although the paper depicts the patients with side effect in impassive clinical terms, doctors who have seen them paint a much different picture. Paul. E. Greene, a neurologist at Columbia University's College of Physicians and Surgeons and a researcher in the study, said the uncontrollable movements some patients suffer are "absolutely devastating."
"They chew constantly, their fingers go up and down, their wrists flex and distend," he said. And the patients writhe and twist, jerk their heads, fling their arms about."It was tragic, catastrophic," Greene said. "It's a real nightmare. And we can't selectively turn it off."
One man was so badly affected that he could no longer eat and had to use a feeding tube, Greene said. In another, the condition came and went unpredictably throughout the day, and when it occurred, the man's speech was unintelligible.
For now, Greene said, his position is clear: "No more fetal transplants. We are absolutely and adamantly convinced that this should be considered for research only. And whether it should be research in people is an open question."
Gerard D. Fischbach, who was director of the National Institutes of Neurological Disorders and Stroke, which sponsored the study and is now dean of the faculty of medicine at Columbia University's College of Physicians and Surgeons said that while the operation had been promoted by some neurosurgeons as miraculous, this was the first time it was rigorously evaluated, using sham surgery as a comparison. Fischbach was the director of the institute only at the end of the study.
"Ad hoc reports of spectacular results can always occur," Fischbach said. "But if you do these studies systematically, this is the result you get."
In the study, researchers led by Curt R. Freed of the University of Colorado Health Sciences Center in Denver and Stanley Fahn of Columbia University's College of Physicians and Surgeons, recruited 40 patients, aged 34 to 75, who had Parkinson's disease for an average of 14 years. The patients were randomly assigned to have substantia nigra cells from four fetuses implanted in their brains or to have sham surgery for comparison.
The surgery took place in Colorado and the patients were evaluated in New York. The fetal cell surgery involved drilling four small holes in the patient's forehead and then inserting long needles through the holes into the brain and injecting the fetal cells. The sham surgery involved drilling the holes but not injecting needles into the brain.
The study's primary measure of success was whether the patients themselves noticed that they were better, as determined by a survey that they mailed in a year later but before they knew whether they had fetal cell implants or not. The study found no difference between the two groups - neither those who had the fetal cell operation nor those who had the sham surgery noticed an improvement in their symptoms.
__________________
Monday, March 30, 2009
23andMe already testing for rare Parkinson's mutations?
23andMe already testing for rare Parkinson's mutations?
Posted on: March 23, 2009 9:15 AM, by Daniel MacArthur
This casual aside on a recent post on personal genomics company 23andMe's corporate blog caught my eye:
Mutations in several other genes have also been associated with Parkinson's disease, but these are extremely rare. Many have been found only in one or two families. While these mutations are so rare that they are not covered by 23andMe (to date we have found no customers with any of them), studying them could help scientists better understand the mechanisms of Parkinson's generally... [my emphasis]
In other words, the company already has probes on its custom chip targeting these variants, but it isn't yet reporting results back to customers.
Why isn't it reporting back? If you'd asked me a couple of months ago, I'd say the motivation was probably to avoid the regulatory hassles associated with testing overtly clinical markers - but the company's willingness to provide results for large-effect variants associated with breast cancer pretty much rules that out.
Instead, the most likely reason to hold back on giving results back to consumers is (perfectly reasonable) caution about the reliability of the test. Screening for extremely rare variants is tricky for two reasons: firstly, since there are very few individuals around who carry the mutation, obtaining positive controls is difficult; and secondly, screening accuracy needs to be extremely high to keep down the rate of false positives.
To illustrate that last point, let's say there was a genetic variant with a population frequency of just 0.1% (1 in every 1000 people carry it)*. Now, let's say you have a test with false positive and false negative rates of just 1 in every 1000 tests, and you run that test on one million people. Of the 1000 carriers in the population, the test will only miss one; but it will also give a positive result for 999 people who are non-carriers. In other words, even for this extremely accurate hypothetical test, only 50% of the people who test positive are actually carriers.
This means that testing for rare variants requires exceptionally high standards of accuracy, probably higher than could reasonably be expected from chip-based assays. Given the risks of reporting potentially unreliable results back to customers for serious risk variants it makes good sense for 23andMe to hold off until it has developed extra assays for quality control; and it's unlikely to do this until it has seen at least a few customers who actually do test positive for the variant in question.
As for obtaining samples from real carriers to enable the development of validation assays: what better way to do that than to recruit 10,000 customers suffering from Parkinson's? Targeted recruitment of customers with other diseases will no doubt follow.
It is now abundantly clear that 23andMe is intent on moving into the overtly clinical domain; Navigenics' purchase of its Affymetrix testing lab and deCODE's move into disease-specific genetic tests are other signs that this is a shift that will involve the entire personal genomics industry.
Personal genomics is getting serious.
Posted on: March 23, 2009 9:15 AM, by Daniel MacArthur
This casual aside on a recent post on personal genomics company 23andMe's corporate blog caught my eye:
Mutations in several other genes have also been associated with Parkinson's disease, but these are extremely rare. Many have been found only in one or two families. While these mutations are so rare that they are not covered by 23andMe (to date we have found no customers with any of them), studying them could help scientists better understand the mechanisms of Parkinson's generally... [my emphasis]
In other words, the company already has probes on its custom chip targeting these variants, but it isn't yet reporting results back to customers.
Why isn't it reporting back? If you'd asked me a couple of months ago, I'd say the motivation was probably to avoid the regulatory hassles associated with testing overtly clinical markers - but the company's willingness to provide results for large-effect variants associated with breast cancer pretty much rules that out.
Instead, the most likely reason to hold back on giving results back to consumers is (perfectly reasonable) caution about the reliability of the test. Screening for extremely rare variants is tricky for two reasons: firstly, since there are very few individuals around who carry the mutation, obtaining positive controls is difficult; and secondly, screening accuracy needs to be extremely high to keep down the rate of false positives.
To illustrate that last point, let's say there was a genetic variant with a population frequency of just 0.1% (1 in every 1000 people carry it)*. Now, let's say you have a test with false positive and false negative rates of just 1 in every 1000 tests, and you run that test on one million people. Of the 1000 carriers in the population, the test will only miss one; but it will also give a positive result for 999 people who are non-carriers. In other words, even for this extremely accurate hypothetical test, only 50% of the people who test positive are actually carriers.
This means that testing for rare variants requires exceptionally high standards of accuracy, probably higher than could reasonably be expected from chip-based assays. Given the risks of reporting potentially unreliable results back to customers for serious risk variants it makes good sense for 23andMe to hold off until it has developed extra assays for quality control; and it's unlikely to do this until it has seen at least a few customers who actually do test positive for the variant in question.
As for obtaining samples from real carriers to enable the development of validation assays: what better way to do that than to recruit 10,000 customers suffering from Parkinson's? Targeted recruitment of customers with other diseases will no doubt follow.
It is now abundantly clear that 23andMe is intent on moving into the overtly clinical domain; Navigenics' purchase of its Affymetrix testing lab and deCODE's move into disease-specific genetic tests are other signs that this is a shift that will involve the entire personal genomics industry.
Personal genomics is getting serious.
Saturday, March 21, 2009
Early Parkinson's Treatment With Rasagiline Safe, Well Tolerated, and Effective Versus Placebo
Early Parkinson's Treatment With Rasagiline Safe, Well Tolerated, and Effective Versus Placebo: Presented at ADPD
By Chris Berrie
PRAGUE, Czech Republic -- March 14, 2009 -- Rasagiline monotherapy is safe and well tolerated, with clinical benefits versus placebo in patients with early, previously untreated Parkinson's disease (PD), researchers noted here at the 9th International Conference on Alzheimer's and Parkinson's Diseases (ADPD).
Early initiation of treatment with rasagiline 1 mg/day also provided significant clinical benefits over later initiation.
A prospective, multicentre study entitled Attenuation of Disease Progression With Azilect Given Once-Daily (ADAGIO) was presented here on March 13 by principal investigator Olivier Rascol, MD, Toulouse University Hospital, Toulouse, France.
"A treatment that slows or halts the progression of disease is a key unmet need in Parkinson's disease," Dr. Rascol stated. He and his colleagues utilised a delayed-start design in their randomised, double-blind, placebo-controlled trial to allow separation of disease-modifying effects from symptomatic effects in the examination of patients with moderate to advanced PD taking rasagiline monotherapy and combination therapy with levodopa.
Patient diagnosis was for cardinal PD signs -- resting tremor, bradykinesia, and rigidity -- with inclusion requiring a disease duration of less than 18 months from diagnosis and investigator judgement of no requirement for additional anti-PD treatment in the following 9 months.
The 1,176 patients enrolled were 61.1% male, with mean baseline characteristics as follows: age, 62.2 years; PD duration, 4.5 months; total Unified PD Rating Scale (UPDRS) score, 20.4; motor-UPDRS score, 14.2; and modified Hoehn and Yahr score, 1.5.
The study followed 2 phases: a 36-week placebo-controlled phase 1, followed by a 36-week full active-treatment phase 2. Randomisation was to 4 groups -- 2 of placebo followed by rasagiline 1 or 2 mg/day for delayed-start treatment (n = 595) and 2 of rasagiline 1 mg/day (n = 288) or 2 mg/day (n = 293) for the full 72 weeks. There were no significant baseline differences across these groups.
With rasagiline 1 mg/day, the 3 specific primary efficacy endpoints were met:
A. The slope in weeks 12-36 of phase 1 was significantly superior with active treatment versus placebo (difference, -0.05; 95% confidence interval [CI], -0.08 to -0.01; P = .0133).
B. Results from the early-start group were significantly superior to those of the late-start group at week 72 (difference, -1.7; 95% CI, -3.15 to -0.21; P = .025).
C. The noninferiority of the slope of early versus late start was met (difference, 0.0; 90% CI, -0.04 to 0.04; P < .0001).
The rasagiline 2-mg/day treatment showed significant benefit in phase 1 versus placebo (P < .001), but did not show superiority versus the delayed start at the end of phase 2.
The secondary endpoint for changes in total UPDRS score from baseline to week 36 for each rasagiline group was met for rasagiline 1 and 2 mg/day, as adjusted effect sizes of -3.0 (95% CI, -3.9 to -2.2; P < .0001) and -3.2 (95% CI, -4.0 to -2.3; P < .0001) respectively.
Rasagiline monotherapy was deemed safe and well tolerated, with few treatment-related adverse events and few discontinuations (placebo, 2.9%; rasagiline 1 mg/day, 3.1%; rasagiline 2 mg/day, 3.8%).
The researchers concluded that this early treatment with rasagiline 1 mg/day is consistent with disease-modifying effects, noting, "ADAGIO also confirms the symptomatic efficacy of rasagiline monotherapy versus placebo in patients with early [Parkinson's] disease."
Funding for this study was provided by Teva Pharmaceutical Industries Ltd. and Teva Neuroscience, Inc.
[Presentation title: The ADAGIO Delayed-Start Study Demonstrates That Early Rasagiline Treatment Slows UPDRS Decline. Abstract P1-423]
By Chris Berrie
PRAGUE, Czech Republic -- March 14, 2009 -- Rasagiline monotherapy is safe and well tolerated, with clinical benefits versus placebo in patients with early, previously untreated Parkinson's disease (PD), researchers noted here at the 9th International Conference on Alzheimer's and Parkinson's Diseases (ADPD).
Early initiation of treatment with rasagiline 1 mg/day also provided significant clinical benefits over later initiation.
A prospective, multicentre study entitled Attenuation of Disease Progression With Azilect Given Once-Daily (ADAGIO) was presented here on March 13 by principal investigator Olivier Rascol, MD, Toulouse University Hospital, Toulouse, France.
"A treatment that slows or halts the progression of disease is a key unmet need in Parkinson's disease," Dr. Rascol stated. He and his colleagues utilised a delayed-start design in their randomised, double-blind, placebo-controlled trial to allow separation of disease-modifying effects from symptomatic effects in the examination of patients with moderate to advanced PD taking rasagiline monotherapy and combination therapy with levodopa.
Patient diagnosis was for cardinal PD signs -- resting tremor, bradykinesia, and rigidity -- with inclusion requiring a disease duration of less than 18 months from diagnosis and investigator judgement of no requirement for additional anti-PD treatment in the following 9 months.
The 1,176 patients enrolled were 61.1% male, with mean baseline characteristics as follows: age, 62.2 years; PD duration, 4.5 months; total Unified PD Rating Scale (UPDRS) score, 20.4; motor-UPDRS score, 14.2; and modified Hoehn and Yahr score, 1.5.
The study followed 2 phases: a 36-week placebo-controlled phase 1, followed by a 36-week full active-treatment phase 2. Randomisation was to 4 groups -- 2 of placebo followed by rasagiline 1 or 2 mg/day for delayed-start treatment (n = 595) and 2 of rasagiline 1 mg/day (n = 288) or 2 mg/day (n = 293) for the full 72 weeks. There were no significant baseline differences across these groups.
With rasagiline 1 mg/day, the 3 specific primary efficacy endpoints were met:
A. The slope in weeks 12-36 of phase 1 was significantly superior with active treatment versus placebo (difference, -0.05; 95% confidence interval [CI], -0.08 to -0.01; P = .0133).
B. Results from the early-start group were significantly superior to those of the late-start group at week 72 (difference, -1.7; 95% CI, -3.15 to -0.21; P = .025).
C. The noninferiority of the slope of early versus late start was met (difference, 0.0; 90% CI, -0.04 to 0.04; P < .0001).
The rasagiline 2-mg/day treatment showed significant benefit in phase 1 versus placebo (P < .001), but did not show superiority versus the delayed start at the end of phase 2.
The secondary endpoint for changes in total UPDRS score from baseline to week 36 for each rasagiline group was met for rasagiline 1 and 2 mg/day, as adjusted effect sizes of -3.0 (95% CI, -3.9 to -2.2; P < .0001) and -3.2 (95% CI, -4.0 to -2.3; P < .0001) respectively.
Rasagiline monotherapy was deemed safe and well tolerated, with few treatment-related adverse events and few discontinuations (placebo, 2.9%; rasagiline 1 mg/day, 3.1%; rasagiline 2 mg/day, 3.8%).
The researchers concluded that this early treatment with rasagiline 1 mg/day is consistent with disease-modifying effects, noting, "ADAGIO also confirms the symptomatic efficacy of rasagiline monotherapy versus placebo in patients with early [Parkinson's] disease."
Funding for this study was provided by Teva Pharmaceutical Industries Ltd. and Teva Neuroscience, Inc.
[Presentation title: The ADAGIO Delayed-Start Study Demonstrates That Early Rasagiline Treatment Slows UPDRS Decline. Abstract P1-423]
Saturday, March 14, 2009
Long Term Results Similar in Two Parkinson's Medications
By Will Dunham
WASHINGTON, March 9 (Reuters) - People with Parkinson's disease may worry over which of two kinds of medications to use when first starting treatment, but a study published on Monday indicates the results are similar either way.
Researchers compared disability levels and quality of life after six years for people who started out taking either the standard generic drug levodopa or privately held German drug maker Boehringer Ingelheim's Mirapex, also called pramipexole.
The two drugs are generally employed as the first line of treatment for Parkinson's disease. In different ways, they address the decline in production of the brain chemical dopamine that occurs with the disease.
Parkinson's undermines control over movements and speech. Patients can have stiffness or rigidity of the arms and legs, slowness or lack of movement, and walking difficulties, along with tremors in their hands, arms, legs, jaw or face.
Levodopa is seen as better to deal with mobility issues and tremors. But it can cause involuntary movements known as dyskinesia, and its effectiveness also may wear off over time.
Mirapex may be less effective at handling motor control symptoms and can cause sleepiness. But it is less likely to cause involuntary movements or lose effectiveness over time.
"Despite a little bit of variations in how people were doing in specific areas, in terms of overall quality of life and disability measurements, the two groups looked the same," University of Rochester Medical Center neurologist Dr. Kevin Biglan, one of the researchers, said in a telephone interview.
"Then it becomes more of an individual decision in terms of short-term issues and individual preferences about some of these complications, potentially," he said.
Mirapex is in a class of drugs called dopamine agonists that also includes GlaxoSmithKline's (GSK.L) (GSK.N) Requip, or ropinirole.
The researchers tracked 222 patients in the study published in the journal Archives of Neurology.
Of those who started on Mirapex, 90 percent of them ended up also taking levodopa, a drug that has been around for more than four decades, Biglan said. But the side effects differed depending on which drug they started on, he added.
"There's been all this research trying to address what's the better initial treatment strategy. And patients have struggled with whether they were making the right decision in terms of what treatment to go with initially," Biglan said.
"So they could probably make a decision regarding either treatment without being overly worried about the long-term implications," he added. Boehringer funded the study. (Editing by Julie Steenhuysen)
WASHINGTON, March 9 (Reuters) - People with Parkinson's disease may worry over which of two kinds of medications to use when first starting treatment, but a study published on Monday indicates the results are similar either way.
Researchers compared disability levels and quality of life after six years for people who started out taking either the standard generic drug levodopa or privately held German drug maker Boehringer Ingelheim's Mirapex, also called pramipexole.
The two drugs are generally employed as the first line of treatment for Parkinson's disease. In different ways, they address the decline in production of the brain chemical dopamine that occurs with the disease.
Parkinson's undermines control over movements and speech. Patients can have stiffness or rigidity of the arms and legs, slowness or lack of movement, and walking difficulties, along with tremors in their hands, arms, legs, jaw or face.
Levodopa is seen as better to deal with mobility issues and tremors. But it can cause involuntary movements known as dyskinesia, and its effectiveness also may wear off over time.
Mirapex may be less effective at handling motor control symptoms and can cause sleepiness. But it is less likely to cause involuntary movements or lose effectiveness over time.
"Despite a little bit of variations in how people were doing in specific areas, in terms of overall quality of life and disability measurements, the two groups looked the same," University of Rochester Medical Center neurologist Dr. Kevin Biglan, one of the researchers, said in a telephone interview.
"Then it becomes more of an individual decision in terms of short-term issues and individual preferences about some of these complications, potentially," he said.
Mirapex is in a class of drugs called dopamine agonists that also includes GlaxoSmithKline's (GSK.L) (GSK.N) Requip, or ropinirole.
The researchers tracked 222 patients in the study published in the journal Archives of Neurology.
Of those who started on Mirapex, 90 percent of them ended up also taking levodopa, a drug that has been around for more than four decades, Biglan said. But the side effects differed depending on which drug they started on, he added.
"There's been all this research trying to address what's the better initial treatment strategy. And patients have struggled with whether they were making the right decision in terms of what treatment to go with initially," Biglan said.
"So they could probably make a decision regarding either treatment without being overly worried about the long-term implications," he added. Boehringer funded the study. (Editing by Julie Steenhuysen)
Saturday, March 7, 2009
NIH awards $4 million to Iowa State veterinary researchers for Parkinson's disease research
NIH awards $4 million to Iowa State veterinary researchers for Parkinson's disease research
Mar 5, 2009
DVM NEWSMAGAZINE
Ames, Iowa- An NIH-affiliated organization recently doled out more than $4 million in grants to two veterinary researchers at Iowa State University (ISU) to further study Parkinson's disease.
The researchers at the Iowa Center for Advanced Neurotoxicology (ICAN) at ISU received the financial support from the National Institute of Neurological Disorders and Stroke (NINDS), a component of the National Institutes of Health (NIH).
The awards represent innovative approaches to funding biomedical research in Parkinson's disease by NINDS, the university reports in a prepared statement.
Dr. Anumantha Kanthasamy, a faculty member in the Department of Biomedical Sciences at ISU's College of Veterinary Medicine and director of ICAN, secured the funding for a new NIH Multi-Principal Investigators Award program. This award is intended to foster interdisciplinary biomedical research among multiple institutions, the university explains.
Kanthasamy will collaborate with Dr. Balaraman Kalayanaraman, chair and professor of the Department of Biophysics at the Medical College of Wisconsin, in developing a novel class of antioxidant-based therapeutic agents for the treatment of Parkinson's Disease. A total of $2.77 million in NIH funding will be provided to their project. ISU will receive about $1.4 million from the award over the next five years.
Dr. Arthi Kanthasamy, another ICAN researcher in neurotoxicology and a faculty member in the Department of Biomedical Sciences at ISU, received an award from the NINDS' New Investigator Award program. She will receive a total of $1.28 million for her work in studying the brain inflammatory mechanisms in Parkinson's Disease models. Arthi Kanthasamy currently researches degenerative processes in stroke models and also teaches pharmacology and histology courses to graduate and veterinary students.
"To receive, not only one, but two awards for work in Parkinson's disease reflects positively on the quality of research being conducted at ISU," says Dr. John Thomson, dean of ISU's College of Veterinary Medicine.
ICAN was created to promote interdisciplinary research related to neurotoxicological problems in both animals and humans. Neurotoxicology bridges the scientific fields of toxicology and neuroscience and plays a key role in the health of humans and animals, the veterinary college reports.
Mar 5, 2009
DVM NEWSMAGAZINE
Ames, Iowa- An NIH-affiliated organization recently doled out more than $4 million in grants to two veterinary researchers at Iowa State University (ISU) to further study Parkinson's disease.
The researchers at the Iowa Center for Advanced Neurotoxicology (ICAN) at ISU received the financial support from the National Institute of Neurological Disorders and Stroke (NINDS), a component of the National Institutes of Health (NIH).
The awards represent innovative approaches to funding biomedical research in Parkinson's disease by NINDS, the university reports in a prepared statement.
Dr. Anumantha Kanthasamy, a faculty member in the Department of Biomedical Sciences at ISU's College of Veterinary Medicine and director of ICAN, secured the funding for a new NIH Multi-Principal Investigators Award program. This award is intended to foster interdisciplinary biomedical research among multiple institutions, the university explains.
Kanthasamy will collaborate with Dr. Balaraman Kalayanaraman, chair and professor of the Department of Biophysics at the Medical College of Wisconsin, in developing a novel class of antioxidant-based therapeutic agents for the treatment of Parkinson's Disease. A total of $2.77 million in NIH funding will be provided to their project. ISU will receive about $1.4 million from the award over the next five years.
Dr. Arthi Kanthasamy, another ICAN researcher in neurotoxicology and a faculty member in the Department of Biomedical Sciences at ISU, received an award from the NINDS' New Investigator Award program. She will receive a total of $1.28 million for her work in studying the brain inflammatory mechanisms in Parkinson's Disease models. Arthi Kanthasamy currently researches degenerative processes in stroke models and also teaches pharmacology and histology courses to graduate and veterinary students.
"To receive, not only one, but two awards for work in Parkinson's disease reflects positively on the quality of research being conducted at ISU," says Dr. John Thomson, dean of ISU's College of Veterinary Medicine.
ICAN was created to promote interdisciplinary research related to neurotoxicological problems in both animals and humans. Neurotoxicology bridges the scientific fields of toxicology and neuroscience and plays a key role in the health of humans and animals, the veterinary college reports.
Wednesday, February 25, 2009
Five Common Complications Often Caused By Parkinsons
As if the diagnosis of Parkinson’s disease is not enough, it is also accompanied by a variety of complications. Some of these problems can be overcome by changing lifestyle habits but others may require the guidance of a doctor or therapist to help cope with them. Not all of these complications can be solved with a shot or pill so expect there to be some frustration as they develop and solutions try to be garnered.
Depression
Sometimes, people develop depression before Parkinson’s disease is diagnosed. The disease affects chemical production in the brain and this includes serotonin and norepinephrine, two chemicals that are associated with depression. When these levels are low or fluctuate on a continuing basis, this can affect mood.
Chewing and Swallowing
As Parkinson’s disease progresses, so does the sluggish movements, limb rigidity and hindered progress of other muscles, including those used in conjunction with the autonomic nervous system. In other words, involuntary movements such as swallowing saliva (and thus food) can be a problem. Chewing can be particularly tough later in the disease thereby requiring softer foods that are easier to get down.
Sexual problems
Decrease in libido is a detrimental side effect to Parkinson’s disease as this can affect personal relationships with a partner or spouse. This loss of sexual desire can be attributed to both mental and physical factors. Depression and chemical imbalances can happen in the brain, causing a decrease in sex. Physically, motor coordination becomes a problem later in the disease as does limb rigidity and the ability to control certain movements.
Sleep problems
Insomnia can occur at night with Parkinson’s patients as well as fits of daytime sleeping and drowsiness. During the night, patients may not be able to fall asleep or if they do, sleep is punctuated by nightmares, uncomfortable feelings in the limbs (such as restless legs syndrome), acting out while dreaming and more.
Body elimination
Bowel and urinary elimination can also be punctuated with problems due to Parkinson’s. Just like with chewing and swallowing, body elimination is a function of the autonomic nervous system, not something consciously thought about but the body performs on its own such as digestion and the creation of fecal and urine matter. The only control a person has is over the different sphincter muscles that are employed to hold in body elimination until a person can get to the bathroom.
It is these sphincter muscles that can be affected. Sometimes, they relax too much causing bladder or bowel incontinence while other times, they are hard to relax so a person has trouble eliminating at all. Constipation is a problem because Parkinson’s can slow digestion and cause the stomach not to empty properly into the intestines. Disease medications can contribute to both urinary and bowel incontinence.
Certain Parkinson’s medications can cause problems with a number of other issues as well. Blood pressure may fluctuate as well as overall drowsiness. Twitching and jerking may occur as well as hallucinations, dry mouth and more. Because each person’s body chemistry is different, there is no way to predict how someone will react to medication, so it is important to be prepared to experiment until the right combination of drugs works positively on symptoms.
Tuesday, February 17, 2009
Study of ways to treat Parkinson’s disease
Grant award for therapy research
Published: 04/02/2009
NEW ways of treating Parkinson’s disease are to be investigated by a researcher at St Andrews University.
Professor Philip Winn, of the school of psychology, has been awarded a grant by the Medical Research Council to study new ways of using an existing therapy.
Deep brain stimulation is a surgical method already used to treat the disease’s symptoms.
These include tremors, difficulty with movements, poor balance and gait disturbance.
With deep brain stimulation, patients can turn on or off electrodes surgically implanted in their brains which send pulses of electricity directly to specific areas of the brain.
The first aim of the research is to understand exactly what happens to brain physiology when the electrodes are switched on, to help develop better methods of stimulation.
The team also hopes to identify other targets in the brain where this stimulation might offer different benefits.
Stimulation at some sites might relieve tremor, while others may have more effect on postural and gait problems.
Prof Winn said: “It is a unique opportunity to integrate basic and clinical science.
“The method is especially useful in cases of Parkinson's where drug treatments are having less effect than normal."
The three-year £1.2million grant brings together teams of researchers in Germany, Italy, France and Scotland, co-ordinated by Christian- Albrechts University in Kiel, Germany, one of the leading centres for the surgical treatment of Parkinson’s.
Thursday, February 12, 2009
Scientists Re-Examine a Treatment for Parkinson's Disease
| 02 February 2009 |
VOICE ONE:
This is SCIENCE IN THE NEWS, in VOA Special English. I'm Bob Doughty.
VOICE TWO:
And, I'm Shirley Griffith. This week, we will tell about what is said to be the largest study yet of a treatment for Parkinson's disease. We will also tell about a study of young Americans and their use of social Web sites on the Internet.
(MUSIC)
VOICE ONE:
Parkinson's is a disease of the central nervous system. The disease affects between five hundred thousand and one million five hundred thousand Americans. Doctors confirm about sixty thousand new Parkinson's cases in the United States each year. The disease affects a small area of cells in the middle of the brain. The cells slowly lose their ability to produce a chemical called dopamine.
The decrease in the amount of dopamine can result in one or more of the general signs of Parkinson's. These include shaking in the hands, arms and legs. They also include muscle tightness and restricted movements. Another symptom is difficulty keeping balanced while standing or walking. Medicine can help patients. Yet it can become less effective as the disease progresses.
VOICE TWO:
Deep brain stimulation uses electricity to shock the brain in areas that help send messages to the body. In Parkinson's patients, these areas of the brain can become blocked. When this happens, the messages give misinformation to the body.
Deep brain stimulation begins by doctors drilling two small holes in the head of the patient. Two thin, electrical wires are then placed in the brain. They are connected under the skin to another wire that leads to a small battery placed in the chest. The device supplies electricity.
Doctors do not know exactly how the brain stimulation works to help patients with Parkinson's. But experts believe the electrical current might help activate nerve cells that are not working correctly.
VOICE ONE:
The study involved two hundred fifty-five Parkinson's patients. It took place at thirteen medical centers across the United States between May of two thousand two and October of two thousand five. The patients kept written records of their physical abilities.
The Journal of the American Medical Association published results of the study. They showed that patients who received deep brain stimulation had better control of their symptoms than those who only took medicine. In fact, the patients who had the treatment reported an average gain of nearly five hours each day of good control of their symptoms. The average gain was zero hours for the other group.
VOICE TWO:
Deep brain stimulation is not the answer for all Parkinson's patients. Doctors say it is best for patients whose medicines cause side effects or are not working. The treatment is not new. It was first approved for use in the United States in nineteen ninety-seven. However, its effectiveness had never before been compared to that of medicines in a large study.
In the United States, Parkinson's patients can receive deep brain stimulation at about three hundred medical centers. The treatment has been performed about forty thousand times throughout the world.
But several possible side effects make the treatment risky. The side effects include pain in the head, problems speaking and slowed movement. One patient who had the surgery died. However, in many cases, the researchers found the side effects ended within six months. And, some patients said the improvements they experienced were worth the risk.
VOICE ONE:
Deep brain stimulation is also costly. It can cost as much as one hundred fifty thousand dollars. In addition, the battery placed under the skin may require a replacement. This means doctors need to perform another operation.
The company that makes the device, Medtronic, helped to pay for the study. Financial support also came from the United States Department of Veterans Affairs and the National Institute of Neurological Disorders and Stroke.
In addition to people with Parkinson's, the treatment is also being tested for patients with severe depression, lasting pain and epilepsy.
(MUSIC)
Thursday, February 5, 2009
Parkinsons Medicine, How We Use It To Treat Parkinsons Disease
To date, there is no known cure for Parkinson’s, despite the ongoing research efforts of scientists across the world. Having said that, there are a number of treatments available which can substantially relieve the pain many patients feel as a result of the symptoms of the disease. It is not the case that every patient will require medication and drugs to treat their condition, and these will only be administered where the severity of the symptoms has a strong adverse affect on the patient’s lifestyle. The course of Parkinsons Medicine offered to a patient will vary with the amount of disruption the symptoms cause, the state of the patient’s condition and the severity of the condition within the patient. Even in these cases, it is not always a guarantee that the symptoms will be helped, although these treatments will go someway to making life more comfortable.
The most effective treatment for the symptoms of Parkinson’s Disease by a long shot is the drug levodopa. This is derived from a naturally produced chemical in plant matter and animals, and works with the nerve cells to produce the dopamine which has been eroded by the patient’s condition, and is thought to be an underlying cause of the disease. The drug allows the majority of patients to extend the period of time in which they can lead their normal lives, effectively stalling the development of their Parkinson’s. Unfortunately, this treatment is only really effective in helping rigidity and bradykinesia, and may be of no help to the tremor or balance problems the patient may be experiencing. The drug is so effective, many patients forgot they are suffering from the disease as they continue to lead their lives as normal. However, levodopa is only a short term solution, as it can never replace the nerve cells which have been irretrievably damaged within the brain.
As with most medications, there are a number of side effects with levodopa, including restlessness, low blood pressure and vomiting. In some cases patients may also occasionally feel confused as to their surroundings , although this is a rare occurrence. It is important for physicians and patients to work together to come up with a happy medium between the benefits and side effects when using levodopa.
When combined with the drug tolcapone, Parkinsons medicine significantly reduces the effects of the disease, and helps block the destruction of dopamine which worsens the condition. Having said that, this tends to increase involuntary movement and twitching over a long course of treatment, and is sometimes withdrawn for several days at a time to ensure its continued effectiveness. However, patients should never completely cease treatment with levodopa without their physician’s guidance, due to the extreme and serious side effects that can emerge as a result.
Although there is no cure for the disease, Parkinsons medicine can go a long way to suppressing the debilitating and disabling symptoms of the condition, and making life more bearable for the many thousands of sufferers around the world.
Clive Jenkins recommends the Parkinsons Disease Help Online website which provides comprehensive information on all aspects of Parkinson’s Disease. To find articles, tips and free information and advice check out the site here:
http://www.parkinsonsdiseasehelponline.com/
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