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.
Monday, March 30, 2009
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)
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