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
Wednesday, November 4, 2009
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
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