News Stories of Interest.....

 

  New Study Results

  Fair Warning

  FOXFLASH

  Hopeful results

  Neurotrophic Growth Factors

  Treadmill Walking

  5 new Parkinson’s genes

  And older articles of interest.....

 

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Importance of Strong NIH Research Funding Shown in New Study Results On Feb. 2, 2012, The New York Times ran a story on its front page about a new Alzheimer's study that scientists believe may have implications for Parkinson's research: Path is Found for the Spread of Alzheimer's (pdf version) An excerpt of particular interest to the Parkinson's community includes the following: "Alzheimer's disease seems to spread like an infection from brain cell to brain cell, two new studies in mice have found. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau. The surprising finding answers a longstanding question and has immediate implications for developing treatments, researchers said. And they suspect that other degenerative brain diseases like Parkinson's may spread in a similar way." We are sending this article to you not only because this is an exciting new discovery, but also because it shows the importance of long-term biomedical research funding. Two researchers cited in the news story – Dr. Scott A. Small and Dr. Bradley T. Hyman – have received funding from the National Institutes for Health (NIH) for their work in this field. Dr. Samuel Gandy, who is quoted in the article as an expert, has received NIH funding since 1986 for his work. Findings like this illustrate why the Parkinson's Action Network continues to fight for strong federal funding and support for biomedical research at the National Institutes of Health. Take Action With PAN Action Alerts! E-mail your Senators: Repeal Medicare Therapy Caps! E-mail your Representative: Repeal Medicare Therapy Caps!

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Common Household Solvent Linked to Parkinson’s Disease

FairWarning - A chemical often found in groundwater and widely used in household products, including spot removers and carpet cleaning fluids, has been linked in a new study to Parkinson’s disease.

The study, which appeared in the Annals of Neurology medical journal, focused on 99 sets of twins. In each case one of the twins suffered from Parkinson’s and the other did not.

Researchers, led by scientists from The Parkinson’s Institute and Clinical Center in Sunnyvale, Calif., asked the twins about their job histories and hobbies, and determined what the twins’ exposure in those settings would have been to six common solvents.

Based on those evaluations, the researchers found a strong link between Parkinson’s and exposure to trichloroethylene, or TCE. They concluded that people who worked with TCE had more than a six times greater risk of developing Parkinson’s, a neurodegenerative disease estimated to afflict as many as 500,000 Americans. Symptoms of Parkinson’s include limb tremors, slowed movement and speech impairment.

As a news release from the Annals of Neurology noted, researchers also found that people exposed to two other solvents — perchloroethylene, or PERC, and carbon tetrachloride, or CCI4 — “tended toward significant risk of develping the disease.”

“Our study confirms that common environmental contaminants may increase the risk of developing PD, which has considerable public health implications,” said one of the leaders of the study, Dr. Samuel M. Goldman of The Parkinson’s Institute.

Goldman said his research team’s findings and previous reports “suggest a lag time of up to 40 years” between TCE exposure and the onset of Parkinson’s, “providing a critical window of opportunity to potentially slow the disease process before clinical symptoms appear.”

Still, he warned that exposure to TCE is pervasive, and doesn’t just occur in the kinds of settings he and his colleagues examined.

According to the journal news release and a fact sheet from The Parkinson’s Institute, TCE still is commonly found in such substances as dry-cleaning solutions, carpet cleaners, adhesives and paints, and as a grease-removing material in industry. That wide use comes even though the Environmental Protectional Agency delcared it a human carcinogen in September, and despite the 1977 decision by the Food and Drug Administration to ban the use of TCE as a general anesthetic, skin disinfectant and coffee decaffeinating agent.

The researchers called TCE the most common organic contaminant found in groundwater, and said it is detected in up to 30 percent of drinking water supplies in the country. It also is found in soil and in the air.

Northwest Parkinson's Foundation news

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INHALED LEVODOPA COULD PROVIDE LASTING RELIEF TO PATIENTS

December 23, 2011...Challenges associated with today’s delivery of levodopa are believed to play a major role in the debilitating motor fluctuations, or “on and off periods,” associated with long-term use of levodopa. Many patients struggle to maintain adequate therapeutic levels of the drug. They endure dyskinesias when levodopa levels are at their highest, followed by periods of poor mobility when the medication wears off between doses. The Foundation has made it a priority to drive research that can solve these problems and offer patients better quality of life.

Civitas Therapeutics’ drug candidate has shown promise in pre-clinical models of PD to produce rapid, consistent and durable relief from these “on and off periods.” As the project moves into the clinical phase, the Foundation is optimistic that it could open up new opportunities to improve the standard of care for those living with PD. Enrollment is expected to begin in 2012.

To learn more, read the Civitas press release or the grant abstract.

 

 

 

FDA COMMITTEE ADVISES AGAINST LABEL CHANGE FOR RASAGILINE (AZILECT)

 (October 17), in a story highlighting the need for a biomarker to measure the progression of Parkinson’s disease and the efficacy of potential new treatments, an FDA advisory committee recommended against a label change for the drug rasagiline (brand name Azilect). The drugmaker, Teva Neuroscience, wanted the FDA to state that Azilect “modifies the clinical progression of Parkinson’s disease” — meaning individuals taking the drug would have a slower progression of symptoms compared to people not treated with the drug. The committee found that there isn’t enough scientific evidence to support this claim. Azilect remains available as a symptomatic treatment for PD.

While any progress toward a disease-modifying therapy is positive, and while the data presented by Teva was compelling, MJFF and five other Parkinson’s organizations issued a joint statement agreeing with the FDA that the jury is still out on rasagiline's ability to slow PD symptoms' progression. For in-depth analysis on the decision and what it means for Parkinson’s patients and researchers, read our News in Context Q&A with Ken Marek, MD, principal investigator of PPMI, a landmark clinical study sponsored by MJFF to identify PD biomarkers.

WWW.MICHAELJFOX.ORG

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Virus destroys Parkinson's symptoms

YourNewsNow - Parkinson's disease is a progressive disorder of the nervous system that affects movement. It develops gradually, and often starts with a barely noticeable tremor in one hand. While tremors may be the most well-known sign of Parkinson's disease, the disorder also commonly causes a slowing or freezing of movement.

According to the Mayo Clinic, there's no cure for Parkinson's disease, but medications can help control some of the symptoms of Parkinson's disease, and in some cases, surgery may be helpful.

A small region deep within the brain is the source for the symptoms of Parkinson's disease. When brain neurons in that region of the brain begin to die, the cells can no longer manufacture the molecule dopamine -- a chemical critical for controlling movement.

The exact cause of Parkinson's disease is unknown, but several factors appear to play a role, including genes. Researchers have found specific genetic mutations that likely play a role in Parkinson's disease. In addition, scientists suspect that many more changes in genes -- whether inherited or caused by an environmental exposure -- may be responsible for Parkinson's disease. Exposure to toxins or certain viruses may trigger Parkinson's signs and symptoms.

For the first time, gene therapy has proven successful in Parkinson's patients. The therapy uses a virus that is stripped of its infectious properties and delivered with a thin tube into the brain's subthalamic nucleus -- a structure "the size of a pine nut" that is involved with movement.

Researchers followed 45 patients for six months after the procedure at seven U.S. medical centers. Half the patients showed improvements early on, which they still sustained six months later.

Most current therapies and research approaches target dopamine to treat motor symptoms associated with Parkinson's disease. In contrast, the focus of the current gene therapy strategy is on increasing GABA -- a brain neurotransmitter that regulates movement.

In Parkinson's disease, GABA is reduced in the area of the brain known as the subthalamic nucleus, causing it to be overactive. Investigators feel this might be a better way to help advanced Parkinson's disease.

(SOURCE: Henry Ford Health System, and Northwest Parkinson's Foundation) 

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A Need To Know Resource from the Michael J. Fox Foundation

Trophic Factors: Specialized Proteins that Nurture and Protect Neuron

What are trophic factors?

Trophic factors (also neurotrophic factors or growth factors) are proteins that promote the survival, growth and function of neurons in the brain. Because the degeneration of dopamine neurons is the pathological hallmark of Parkinson's disease, these proteins are of great interest to Parkinson's researchers. During normal brain development, trophic factors are critical for the correct wiring of the nervous system. Trophic factors that have received significant attention in Parkinson's research include GDNF and the closely related neurturin.

Why are trophic factors important?

The word "trophic" comes down to English from a Greek word meaning "to nourish." This goes a long way toward describing what neurotrophic factors do for neurons: enhance function and prevent death.

In preclinical models of Parkinson's disease, trophic factors have been shown to promote the survival of dopamine neurons, as well as to induce these neurons' regrowth, or sprouting. The molecular effects seen in the brain were accompanied by an outward improvement in motor symptoms. These promising preclinical results have led to the investigation of trophic factors as potential neuroprotective PD therapies.

What stands in the way of trophic factor therapies?

One of the greatest challenges to the development of trophic factor therapies is finding a viable delivery approach. Trophic factors are proteins, which cannot be given orally (in pill or liquid form) because they are degraded in the stomach or intestine. They also do not readily cross the blood-brain barrier. This barrier protects the brain by preventing certain molecules, including almost all proteins, from passing from the blood stream into brain tissue. However, it also creates an obstacle to peripheral administration of some neurological therapies, including trophic factors. Since trophic factors don't cross the blood-brain barrier, they can work only when injected into or produced inside of the brain. To advance trophic factors as a viable therapy, researchers must develop technologies to overcome the blood-brain barrier impediment.

What recent attempts have been made to deliver trophic factors to the brain?

Technologies that optimize the diffusion and spread of trophic factors into brain tissue are in varying stages of development, and some have already been tested in clinical trials in PD patients.

• Direct brain infusion. Catheters are implanted directly into the brain. The catheters are attached to pumps that control infusion of the trophic factor. The most promising approaches involve direct infusion into the putamen, the brain region marked by loss of dopamine in PD. The rate of infusion can be closely controlled, and treatment can be discontinued if adverse events occur. The surgery is highly invasive, however, and patients must keep the catheters in place for the duration of treatment. Additionally, this approach is subject to possible immunological responses, primarily development of antibodies that might block the function of protein, resulting from protein leakage from the pumps and infusion of foreign proteins.

  Direct brain infusion of the trophic factor GDNF has been tested in four separate clinical trials to date, with varying degrees of success. While positive clinical outcomes were observed in two open-label clinical studies, this result was not replicated in a subsequent double-blind study. Researchers are continuing to work to understand the differences in results between these studies and to optimize testing of future direct brain infusion approaches.

• Gene therapy approaches. This approach involves injecting a "viral vector" (a virus that has been engineered not to cause illness) containing the gene that expresses the trophic factor directly into the patient's putamen, the part of the brain where dopamine neurons send their signals. If successful, this injection causes the patient's own brain tissue to begin producing the trophic factor. The extent of trophic factor expression in the brain is determined by the amount of virus injected and the location and number of these injections.

  This approach can achieve high levels of localized trophic factor production. Additionally, having the patient's own cells produce the trophic factor reduces the risk of immunological responses to the treatment. But a major limitation of this approach is that with current technologies, there is no way to regulate expression of the trophic factor once the virus is injected. Additional efforts are under way to develop "regulatable" gene therapy approaches - which would make it possible to "turn off" or otherwise control a gene in case of adverse effects following implantation.

  Additionally, The Michael J. Fox Foundation has provided funding for Ceregene Inc.'s Phase I and Phase II clinical trials to test gene therapy delivery of neurturin, a trophic factor closely related to GDNF. Following positive safety results from the Phase I trial, reported in fall 2006, the Foundation signed on to support the Phase II clinical trial, currently under way.

• Stem-cell-based delivery. Stem cells are engineered to produce trophic factors and are then injected into the brain. An example of one such delivery approach uses neural stem cells engineered to produce GDNF, then injected into the putamen. This approach harbors certain advantages - neural stem cells may produce additional positive factors beyond GDNF, and once injected, stem cells may migrate in the brain to increase diffusion of GDNF into brain tissue. There are limitations to this approach, however, similar to those seen in gene therapy: Patients bodies' may reject the stem cells, and there is an overall lack of ability to control the stem cells once they are injected. This approach is currently in preclinical development working toward a clinical trial.

• Encapsulated cell technology (ECT). A current LEAPS award from MJFF is funding exploration of ECT as an alternative delivery system for GDNF. How it works: Cells engineered to produce GDNF are enclosed in a non-biodegradable capsule, which is then implanted into the putamen. Because the capsule is non-biodegradable, the patient's brain is less likely to reject the foreign cells; the GDNF passes through the capsule, however, for the primary purpose of protecting dopamine neurons and stimulating their regeneration. This approach can achieve highly localized trophic factor production. An additional advantage is that the capsule can be removed if adverse events develop. Like other approaches, however, ECT is subject to possible immunological responses including rejection. It is also not clear whether sufficient levels of GDNF can be delivered through this approach.

What is the MJFF view on trophic factors?

Trophic factors represent one of the most promising approaches to develop neuroprotective and neurorestorative therapies in the short term. Determining the efficacy of trophic factors, as well as optimizing various delivery strategies, are research priorities for MJFF.

Compelling preclinical data supports clinical development of GDNF and neurturin. Additional trophic factors also have been discovered and should also be vigorously pursued as potential PD therapies. With the establishment of reliable and safe delivery approaches, we are optimistic that trophic factor therapy will become a viable treatment option for PD patients

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Treadmill Walking Improves Parkinson's Symptoms

Low-Intensity Treadmill Training Helps Parkinson's Patients' Gait, Mobility
 - People with Parkinson’s disease who walk on a treadmill at a comfortable, low-intensity speed may be able to improve their gait and mobility, new research indicates.

Such exercise may be better than walking at faster speeds for a shorter period of time or resistance training that includes leg-press repetitions, curls, and extensions, according to researchers from the University of Maryland.

In the first randomized trial of its kind, researchers enrolled 67 Parkinson’s disease patients who had trouble walking and assigned them to three types of exercise.

Different Groups in Study
One group did high-intensity treadmill walking, walking at faster speeds but for a shorter duration of 30 minutes. Another group walked on a treadmill at slower speeds, but for a longer period of 50 minutes. The third group stretched and performed other resistance exercises, including repetitions of leg presses, extensions, and curls.

All participants exercised three times a week for three months, supervised by exercise physiologists at the Baltimore VA Medical Center.

The study results indicate that low-intensity treadmill training resulted in the most consistent improvements in gait and mobility. People who trained with low-intensity walking performed better than people in the other two groups on distance and speed tests.

Only stretching and resistance training improved scores on a standard Parkinson’s disease performance measure, called the Unified Parkinson’s Disease Rating Scale.

Low-Intensity Exercise
“Contrary to evidence suggesting that high-intensity exercise is the most effective, our results suggest that a combination of low-intensity training and stretching-resistance training may achieve the greatest improvements for people with Parkinson’s disease,” Lisa M. Shulman, MD, of the University of Maryland, says in a news release. “These results have important implications for how we manage Parkinson’s disease, since low-intensity exercise can be done by most people with Parkinson’s, and our patients frequently ask what type of exercise they should be doing.”

Bill Hendrick, WebMD and the Northwest Parkinson's Foundation

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LONDON — Scientists have identified five new genes linked to Parkinson’s disease in a large genetic analysis of the illness, according to a new study.

After reviewing nearly eight million possible genetic mutations, researchers pinpointed five genes connected to Parkinson’s disease. Previously, six other genes were identified, and experts say there is now increasing proof the degenerative disease is sparked by peoples’ genes.The discovery doesn’t mean there are any new treatments just yet, but experts are optimistic they are getting closer.

“The major common genetic variants for Parkinson’s have been found,” said Nick Wood, a professor at the Institute of Neurology at University College London, one of the researchers who led the study. “We haven’t put together all the pieces of the puzzle yet, but we’re not that far off,” he said. He predicted a diagnostic test might be ready within a few years.

Until recently, scientists hadn’t been sure what caused Parkinson’s disease, but assumed environmental factors such as exposure to chemicals or past head injuries were largely to blame. Scientists analyzed genetic samples from more than 12,000 people with Parkinson’s disease and more than 21,000 from the general population in Europe and the U.S.  They found people with the highest number of mutations in the 11 genes linked to Parkinson’s were two-and-a-half times more likely to develop the disease than people who had the least amount of mutations. The average person has a 2.5 per cent chance of developing Parkinson’s disease in their lifetime, and the risk for people whose close relatives have the illness is about six per cent.

The research was paid for by the Wellcome Trust, the National Institute of Aging and the U.S. Department of Defense. It was published online Wednesday in the medical journal Lancet.In an accompanying commentary, scientists said identifying Parkinson’s genes could help explain what triggers the disease and one day lead to new treatments.

“There is good reason for optimism that these advances will be translated into direct benefits for our patients,” wrote Christine Klein and Andreas Ziegler of the University of Lubeck in Germany.

MJFF Impact Report: Dyskinesia

MJFF Impact Report: Dyskinesia

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Parkinson’s disease power switch located

October 06, 2010

In a transformative new study, U.S. researchers have uncovered both the key cause and a promising treatment for Parkinson’s disease. The degenerative movement disorder occurs when the tiny power plants that fuel afflicted brain cells are turned off, the Harvard University-led study has found. This power outage may well be reversed by medications that throw a master switch gene controlling the energy-producing cell structures back on, the paper suggests.

“It’s all very exciting . . . because I think it is potentially a breakthrough in Parkinson’s disease,” says Dr. Anthony Phillips, head of neurosciences with the Canadian Institutes of Health Research. “It’s really coming together nicely. I think it is very, very promising and I think it will get a lot of interest.”

Dr. Clemens Scherzer, the senior paper author, likens the key gene he has identified – known as PGC-1alpha — to the main breaker in a basement electrical console. “This would be the main power switch that turns everything back on,” says Scherzer, a Harvard neurologist.

Importantly, Scherzer says, there are already approved drugs available that are turning the same genetic master switch on in other diseases like diabetes.

If these drugs can hit the switch in brain cells, as Phillips says is likely, it could provide a treatment that would ward off or reverse the ailment’s crippling onslaught in its earliest stages.

Scherzer says that all the genes that control the energy-producing machinery of a cell – churning structures known as mitochondria – are turned off in Parkinson’s disease.  These mitochondria are divided into five power cells, each of which is genetically inactivated in the disease. But all five centres can be reactivated by targeting the master PGC-1alpha gene, Scherzer says. “You can think of it like a power switch that, if you turn on this master regulator you can turn the activity of this energy-producing machinery back on,” he says.

Dr. Timothy Greenamyre, vice chair of neurology at the University of Pittsburgh, calls the identification of a mitochondrial cause a “sea change” in the understanding of the ailment.

“This study was really a tour-de-force and Scherzer brought together a lot of groups and their data sets to do this,” says Greenamyre, a movement disorder expert. “I think he really has to be complimented. This is a very, very solid study.”

Parkinson’s, which affects some 100,000 Canadians and more than 6 million globally, is an attack on dopamine cells in the brain stem, which control motor movements. In the study, Scherzer’s team actually turned tissue samples of these dopamine cells back on by inducing high levels of the master gene into a cultured mix.

“But (the gene) is a very exciting target for medicines because pharmaceutical companies have realized its importance before in diseases that are much more common than Parkinson’s, such as diabetes,” he says. Indeed, there are approved diabetes drugs, and several promising medications now being screened, that appear able to throw the PGC-1alpha switch.

“Pharmaceutical companies can now go back and see whether these drugs or tested compounds can cross into the brain of Parkinson’s patients,” Scherzer says.

Phillips says the likelihood that some of these drugs would cross into the brain is high.

Adds Greenamyre: “I agree there’s that potential and it’s very exciting.”

The study appears in the first anniversary issue of the journal Science Translational Medicine, which features research making the jump from the laboratory to practical usage.

Scherzer thinks a combination of environmental chemicals, like pesticides and manganese, plus a variety of genetic risk factors for the disease combine to cause the ailment. Yet the afflicted, dopamine-producing cells appear to be able to ward these risk factors off when their mitochondria are robust.

Greenamyre’s only caution is that the paper does not definitively show that PGC-1alpha has itself gone off in Parkinson’s disease. “They show that everything that’s controlled by (it) is down, but they don’t show there’s anything wrong with the breaker switch,” he says.

He says it could be imagined the electrical wiring coming out of the main switch is bad, but that the switch itself is working.

Joseph Hall

Health Reporter

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The Parkinson Alliance announces that the results of our Deep Brain Stimulation (DBS) Consensus Conference...held in April 2009, has been published in Archives of Neurology online. 

For anyone who wishes to download this document, please visit the home page of DBS-STN.org.  We have a link on the home page that will take you directly to this report in Archives of Neurology.

If you have any questions, please visit the Forum section at www.dbs-stn.org.  Questions will be answered by several specialists in Movement Disorders, including Jeff Bronstein, MD, PhD, Director of the Movement Disorders Center at UCLA and the main author of this report, among other medical specialists who consult for The Parkinson Alliance.

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New Clinical Trial Begins Ceregene recently launched a new trial for its CERE-120 treatment. Learn more about the trial and hear from Dr. Raymond T. Bartus, Executive Vice President and Chief Scientific Officer at Ceregene, on how you can participate!  Read more.

This Makes Sense.....

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Previously Reported....

Vietnam Vets with Parkinson's Gain Access to Disability Benefits VA Publishes Final Regulation to Aid Vietnam Veterans Exposed to Agent Orange
The Department of Veterans Affairs (VA) today, August 31, published its final regulation establishing Parkinson’s disease, ischemic heart condition, and B-cell leukemias as service-connected disabilities for Vietnam veterans exposed to Agent Orange.  The final regulation grants a 100% disability rating for Parkinson's disease, as well as retroactive veteran and survivor payments for qualifying veterans.

What Does this Mean For Vietnam Vets with PD?

Accessing health care and disability compensation will be easier for qualifying veterans.  If a veteran served in Vietnam from January 9, 1962 to May 7, 1975 and now has been diagnosed with Parkinson’s disease, they are presumed to have been exposed to herbicides.  The veteran does not have to prove an association between their disease and their military service.  The presumption simplifies and speeds up the application process for disability compensation, and all those awarded service-connection will become eligible to join the VA healthcare system.   

The VA will now review approximately 90,000 previously denied claims by Vietnam veterans for service-connection for these three conditions.  Some additional veterans will be eligible for retroactive benefits.  For new claims, VA may pay benefits retroactive to the effective date of the regulation or to one year before the date VA receives the application, whichever is later.  For pending claims and claims that were previously denied, VA may pay benefits retroactive to the date it received the claim.

So When Will This Go Into Effect?

Even though the final regulation is published, the regulation is subject to a 60-day review period by Congress before the VA can begin paying benefits for new claims.

The Senate Veterans Affairs Committee is scheduled to hold a hearing on September 23 to review the rule and to discuss how the VA Secretary makes his decision to establish a disease as a service-connected disability.  There certainly is no intention for Congress to actually block the implementation of the final rule, but the VA will have to wait 60 days before they can start compensating veterans.

What the Final Rule Didn’t Do

The Parkinson’s community sent nearly 400 comments to the VA in support of the proposed regulation.  Many of the comments urged the VA to clarify its definition of Parkinson’s to include diseases of Parkinsonism (primary, atypical, and secondary Parkinsonian syndromes).  Unfortunately, the final rule did not expand the definition of Parkinson’s disease to include Parkinsonism.  VA argues that the current medical evidence does not support the expansion of the definition at this time but will reconsider if the Institute of Medicine (IOM) provides additional guidance in future reports.  

PAN will continue to work with the VA to ensure that all veterans living with Parkinson’s and Parkinsonism receive access to the healthcare and benefits they wholeheartedly deserve.

Apply for Benefits

If you are a Vietnam veteran with Parkinson’s and have not applied for benefits, we encourage you to submit your application for compensation now—even before the VA can start paying claims.  For more information about applying for VA benefits and Agent Orange, visit the VA Web site.

 and...

FOR IMMEDIATE RELEASE                                   

August 30, 2010                                   

VA Publishes Final Regulation to Aid Veterans Exposed to Agent Orange

VA Health Care and Benefits Provided for Many Vietnam Veterans

WASHINGTON – Veterans exposed to herbicides while serving in Vietnam and other areas will have an easier path to access quality health care and qualify for disability compensation under a final regulation that will be published on August 31, 2010 in the Federal Register by the Department of Veterans Affairs (VA).  The new rule expands the list of health problems VA will presume to be related to Agent Orange and other herbicide exposures to add two new conditions and expand one existing category of conditions.

 “Last October, based on the requirements of the Agent Orange Act of 1991 and the Institute of Medicine’s 2008 Update on Agent Orange, I determined that the evidence provided was sufficient to award presumptions of service connection for these three additional diseases,” said Secretary of Veterans Affairs Eric K. Shinseki.  “It was the right decision, and the President and I are proud to finally provide this group of Veterans the care and benefits they have long deserved.”The final regulation follows Shinseki’s determination to expand the list of conditions for which service connection for Vietnam Veterans is presumed. VA is adding Parkinson’s disease and ischemic heart disease and expanding chronic lymphocytic leukemia to include all chronic B cell leukemias, such as hairy cell leukemia.    In practical terms, Veterans who served in Vietnam during the war and who have a “presumed” illness don’t have to prove an association between their  medical problems and their military service.  By helping Veterans overcome evidentiary requirements that might otherwise present significant challenges, this“presump tion” simplifies and speeds up the application process and ensure that Veterans receive the benefits they deserve. The Secretary’s decision to add these presumptives is based on the latest evidence provided in a 2008 independent study by the Institute of Medicine concerning health problems caused by  herbicides like Agent Orange.

Final Regulation  2/2/2

Veterans who served in Vietnam anytime during the period beginning January 9, 1962, and ending on May 7, 1975, are presumed to have been exposed to herbicides.  More than 150,000 Veterans are expected to submit Agent Orange claims in the next 12 to 18 months, many of whom are potentially eligible for retroactive disability payments based on past claims.  Additionally, VA will review approximately 90,000 previously denied claims by Vietnam Veterans for service connection for these conditions.  All those awarded service-connection who are not currently eligible for enrollment into the VA healthcare system will become eligible.This historic regulation is subject to provisions of the Congressional Review Act that require a 60-day Congressional review period before implementation.  After the review period, VA can begin paying benefits for new claims and may award benefits retroactively for earlier periods.  For new claims, VA may pay benefits retroactive to the effective date of the regulation or to one year before the date VA receives the application, whichever is later.  For pending claims and claims that were previously denied, VA may pay benefits retroactive to the date it received the claim.      VA encourages Vietnam Veterans with these three diseases to submit their applications for access to VA health care and compensation now so the agency can begin development of their claims.  Individuals can go to a website at  http://www.vba.va.gov/bln/21/AO/claimherbicide.htm to get an understanding of how to file a claim for presumptive conditions realated to herbicide exposure, as well as what evidence is needed by VA to make a decision about disability compensation or survivors benefits. Additional information about Agent Orange and VA’s services for Veterans exposed to the chemical is available at www.publichealth.va.gov/exposures/agentorange.

The regulation is available on the Office of the Federal Register website at http://www.ofr.gov/. 

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 New Exercise for Parkinson's Patients

CentralPA.com/Charlotte Ames - Pole walking is big with hikers. But now medical researchers are studying whether pole striding can benefit people with Parkinson's disease.

Studies show exercise, especially workouts that target balance and the muscles in the lower limbs, can greatly reduce the risk for falls among older people. Those with Parkinson’s may also benefit from an exercise program. However, rigidity can make exercise difficult. Some patients may also be afraid of falling during exercise.

Arizona researchers are testing the use of walking poles to help Parkinson’s patients with movement and balance problems. Patients can use the poles to maintain balance while walking. Holly Shill, M.D., Neurologist with Banner Sun Health Research Institute in Sun City, AZ, says the poles also provide a bit of an upper extremity workout.

In the current study, Parkinson’s patients are using the poles to exercise for 45 minutes, three days a week. Patients are advised not to compete with one another, but rather to work out at a comfortable intensity, with the goal of getting to a target heart rate.

Darolyn O'Donnell, Recreation Therapy Coordinator with the Muhammad Ali Parkinson Center in Phoenix, AZ, says prior to the start of the class, participants put on heart monitors and pedometers. This allows researchers to monitor the effects of the exercise. Researchers are also performing 3 sets of PET scans on the patients to determine if the exercise program has any favorable changes in brain metabolism.

The current study involves 16 patients. Although the results are not yet known, Schill expects to see some advantages to pole striding. She has observed that Parkinson’s patients who exercise tend to have a better quality of life and slower progression of their disease.

Information provided by the Northwest Parkinson's Foundation... www.nwpf.org

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National Parkinson Foundation Celebrates the Life of Nathan Slewett, 97, Chairman Emeritus

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News Release

SOCIAL SECURITY

Social Security to Provide Helpful Health Care Information

to Over 3 Million Disability Applicants Each Year

Michael J. Astrue, Commissioner of Social Security, today announced the agency is providing helpful health care information and website links to the more than three million individuals who apply each year for Social Security and Supplemental Security Income (SSI) disability benefits. The website links take disability applicants to two U.S. Department of Health and Human Services (HHS) websites – www.healthfinder.gov where they will find information and tools to help them better understand and cope with their conditions; and www.healthfinder.gov/rxdrug where they may be able to get help paying for prescription drugs.

“This year over three million Americans will apply for disability benefits. Whether they meet the statutory test and qualify for benefits or not, almost all of them are facing difficult economic and medical challenges. One of the advantages of our fully electronic system is that our notices can provide applicants with valuable information provided by HHS that might help them make good choices faster,” Commissioner Astrue said. “Twenty five years ago, I had the experience of filing for disability benefits on behalf of my seriously ill father. It would have been a blessing to have had easy access to this kind of important information.”

The website at www.healthfinder.gov provides detailed information about specific diseases. For example, an applicant with breast cancer, rheumatoid arthritis, Alzheimer’s disease, diabetes, or other diseases can go to the site to gather information about diagnosis, symptoms, treatment, ongoing research, and local resources available to people with those diseases. The website at www.healthfinder.gov/rxdrug links people to the Partnership for Prescription Assistance, which directs people to information on reduced cost or free prescription drugs offered by drug companies, state and local governments, and local organizations.

The helpful health care links also are available on Social Security’s website at www.socialsecurity.gov/applyfordisability.

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Older articles of interest..... 

Vaccine Reverses Parkinson's Disease in Pre-clinical Model

On March 1, 2010, researchers funded in part by The Michael J. Fox Foundation announced that they had developed a vaccine that reverses an experimental form of Parkinson’s disease in a pre-clinical model. The Michael J. Fox Foundation spoke with Scientific Advisory Board member David Standaert, MD, PhD, to gain a clearer understanding of the news and what it may mean for people with PD. Dr. Standaert is the John and Juanelle Strain Professor of Neurology and Director, Center for Neurodegeneration and Experimental Therapeutics, at the University of Alabama at Birmingham.
To read the full article, please click here

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Re-Inventing PD Therapy......please click here for a most interesting video

Stimulating Updates…..

Earlier this year Medtronic announced that the FDA approved of  two new Deep Brain Stimulation (DBS) devices that offer programming advances and new tools for patients with movement disorders.

The therapy: DBS delivers small electrical pulses to precisely targeted areas within one or both sides of the brain to help patients achieve greater control over disabling bodymovements.

The new devices…  Activa RC and Activa PC… provide bi-lateral stimulation (to both sides of the brain) and offer a more advanced approach to device programming, and additional tools for capturing history relevant to the patient’s therapy. Per news releases, the new programming options provide greater ability to fine tune the stimulation field and give patients more options to optimize their settings compared to previous DBS devices. Additionally, information about patient symptoms and side effects can be stored in the device, which is helpful to physicians in determining the best programming settings for each patient. These devices also have a hand-held patient programmer, which features new advancements, including an LCD screen that provides valuable information such as the level of battery charge. The programmer allows patients to alternate between stimulation settings pre-programmed by their clinician so they can customize their therapy based on their activity.

Per Leo Verhagen, M.D., Ph.D., medical director of the Surgery Program for Movement Disorders at Rush University Medical Center, Chicago. “This advanced technology will offer more programming features that allow doctors to optimize stimulation effects and also provide options for patients to better control and monitor their therapy settings….and may eliminate the need for frequent battery changes.”

The Activa PC is powered by a primary cell non-rechargeable battery that does not require any regular maintenance from the patient to provide continuous stimulation for multiple years. This  neurostimulator represents a 20 percent reduction in size and weight compared to previous bi-lateral devices and has similar battery life.

The Activa RC is the first rechargeable DBS neurostimulator and lasts for nine years

before replacement is necessary. Patients need to recharge the device at home on a regular basis

depending on their stimulation settings. Activa RC, also significantly smaller than previous bi-lateral

devices.

And there’s more….The Brio….reported to be the world's smallest neurostimulator

The Brio, barely larger than a typical wristwatch, is implanted near the collarbone and sends mild electrical pulses to specific targets in the brain. It is not yet approved for use in the U.S. Weighing in at just 1 ounce and measuring a mere 10 millimeters thick, the Brio is the smallest, longest-lasting rechargeable deep brain stimulator (DBS) that aims to treat the symptoms of Parkinson's in the world, according to its creator. One battery is supposed to survive a decade of recharging.

A 67-year-old man who has suffered from Parkinson's disease since his early 40s has become the first person in the world to be implanted with the Brio neurostimulator, which St. Jude Medical says has just earned CE Mark approval (CE stands for Conformite Europeenne).

(Credit: St. Jude Medical, Elizabeth Armstrong Moore and Rayilyn Brown Arizona Chapter National Parkinson Foundation)

 
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WELL WATER AS A CAUSE OF PARKINSON'S DISEASE

Environmental Health Perspectives [2009] (Nicole M. Gatto, Myles Cockburn, Jeff Bronstein, Angelika D. Manthripragada, and Beate Ritz)

Complete report

Consumption of pesticide contaminated well water has often been claimed to be a cause of Parkinson’s Disease. When researchers investigated consumption of water from private wells in areas with documented historical pesticide use, they found that it was associated with an increased risk of Parkinson's Disease. Six pesticides were examined : diazinon, chlorpyrifos, propargite, paraquat, dimethoate, and methomyl. People with Parkinson's Disease were found to have consumed well water an average of more than four years longer than people that did not have Parkinson's Disease. Consumption of well water contaminated with the pesticides methomyl, chlorpyrifos or propargite resulted in a 70% to 90% increase in the risk of developing Parkinson's Disease. Exposure to a higher number of water soluble pesticides and organophosphate pesticides also increased the risk of causing Parkinson's Disease.

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Aug.. 5, 2009

 Normal brain circuits may cause movement disorder
 
Specific changes in brain pathways may counteract genetic mutations for the movement disorder dystonia, according to new research in the Journal of
Neuroscience. Few people who inherit dystonia genes display symptoms — namely sustained muscle contractions and involuntary gestures — and the study
provides a possible explanation. This result could lead to new treatments for the estimated 500,000 North Americans diagnosed with dystonia. In this study, researchers looked at how brain connections might explain the disorder.

"Our findings begin to show why someone can live with a genetic mutation without ever developing the disease," said David Eidelberg, MD, at The Feinstein Institute for Medical Research, the study's senior author.

Scientists at The Feinstein Institute used an MRI-based approach called diffusion tensor imaging, a technique that maps the connections between structures in the human brain. Twenty patients with mutated genes associated with dystonia were assessed (12 with symptoms, eight without), along with eight healthy patients without these mutations. The authors identified two different brain pathways that determine the severity of symptoms. One pathway connecting the cerebellum with the thalamus is abnormal in all people carrying the mutant gene, and predisposes carriers to dystonia. In the patients with mutated genes but no symptoms, a second pathway between the thalamus and the cortex is also abnormal. Surprisingly, this second pathway is normal in patients with symptoms. The researchers
suggest that in people who have the mutations but no symptoms, the second abnormality may offset the effect of the first, preventing the disease's outward signs.

David Standaert, MD, PhD, at University of Alabama at Birmingham, is an expert in Parkinson's disease and other movement disorders and was not affiliated
with the study. Standaert says that although dystonia is a relatively rare disorder, the study has implications for other neurological illnesses, such as Parkinson's, Alzheimer's, and Huntington's diseases; ataxia and muscular dystrophies; and even forms of migraine.

"The core idea here is that many diseases can be triggered by a single gene, but the expression of this gene can differ greatly, even in individuals from the same family," Standaert said. "Dystonia provides dramatic examples of this. Two siblings may have the same abnormal gene, but one will be severely disabled by twisting and cramping of the muscles, while the other will be essentially normal."

The pathway abnormalities identified in the study could likely have formed in an early stage of brain development, Standaert suggested. Symptoms in adult
life, therefore, may be determined by subtle shifts in early brain growth. Detailed study of these newly implicated pathways in both humans and animals
could lead to ways to prevent symptoms, if balance to the affected pathways is restored.
Source: Society for Neuroscience

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Scoliosis has been found to be far more common in people with Parkinson's Disease

12th July 2009... Scoliosis is an often painful medical condition in which a person's spine is curved from side to side. For more information go to Scoliosis.  Scoliosis was defined as a deviation of the spine of 10 degrees or more. All of the patients submitted to a scanograph to allow measurement of the degree of scoliosis. Scoliosis was found in a third of people with Parkinson's Disease. This is far more common than would be expected. Scoliosis was found to be  seven times more likely in women than it is in men. The likelihood also increased with age.  The use of dopaminergic drugs did not appear to have any effect on the degree of scoliosis. The researchers do not explain this prevalence of scoliosis in Parkinson's Disease, especially in women. However, the excessive muscle contraction that occurs in Parkinson's Disease can cause the upper body to bend towards one side rather than the other.

Viartis/Journal of Clinical Neurology [2009] 5 (2) : 91-94 (Baik JS, Kim JY, Park JH, Han SW, Park JH, Lee MS.)

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Dopamine transporter genetic variants and pesticides in Parkinson's disease

 

Research suggests that independent and joint effects of genetic variability in the dopamine transporter (DAT) locus and pesticides may influence Parkinson's disease (PD) risk. MATERIALS : METHODS: In 324 incident PD patients and 334 population controls from our rural California case-control study, we genotyped rs2652510, rs2550956 (for the DAT 5' clades), and the 3' variable number of tandem repeats (VNTR). Using geographic information system methods, we determined residential exposure to agricultural maneb and paraquat applications. We also collected occupational pesticide use data. Employing logistic regression, we calculated odds ratios (ORs) for clade diplotypes, VNTR genotype, and number of susceptibility (A clade and 9-repeat) alleles and assessed susceptibility allele-pesticide interactions. RESULTS: PD risk was increased separately in DAT A clade diplotype carriers [AA vs. BB: OR = 1.66; 95% confidence interval (CI), 1.08-2.57] and 3' VNTR 9/9 carriers (9/9 vs. 10/10: OR = 1.8; 95% CI, 0.96-3.57), and our data suggest a gene dosing effect. Importantly, high exposure to paraquat and maneb in carriers of one susceptibility allele increased PD risk 3-fold (OR = 2.99; 95% CI, 0.88-10.2), and in carriers of two or more alleles more than 4-fold (OR = 4.53; 95% CI, 1.70-12.1). We obtained similar results for occupational pesticide measures. DISCUSSION: Using two independent pesticide measures, we a) replicated previously reported gene-environment interactions between DAT genetic variants and occupational pesticide exposure in men and b) overcame previous limitations of nonspecific pesticide measures and potential recall bias by employing state records and computer models to estimate residential pesticide exposure. CONCLUSION: Our results suggest that DAT genetic variability and pesticide exposure interact to increase PD risk.

Ritz BR, Manthripragada AD, Costello S, Lincoln SJ, Farrer MJ, Cockburn M, Bronstein J.

Department of Epidemiology, Center for Occupational and Environmental Health, UCLA School of Public Health, University of California at Los Angeles, Los Angeles, California 90095-1772, USA. britz@ucla.edu

PMID: 19590691 [PubMed - in process]

 

 

Viartis provided a summary of the above in a bit more understandable language: The chance of pesticide exposure causing Parkinson's Disease has been found to be far greater in those genetically inclined to Parkinson's Disease. Genetic defects are not typical in Parkinson's Disease. However, those people that have them are usually unaware of them. A defect in the dopamine transporter (DAT) can increase the risk of Parkinson's Disease by more than one and a half times, and as much as several times. The dopamine transporter (DAT) rids dopamine after it is produced. There are usually lower levels of DAT in Parkinson's Disease because there is less dopamine to rid. The researchers do not explain how this defect can increase Parkinson's Disease. However, ridding dopamine too readily would explain the increased prevalence of Parkinson's Disease. In combination with exposure to pesticides, the risk of Parkinson's Disease was multiplied. Exposure to the pesticides paraquat and maneb, which are known causes of Parkinson's Disease, were increased by three times in those people  that had one defect in the dopamine transporter, and by more than four times in those people that had two defects in the dopamine transporter. In some people the risk was many times greater than this.

 

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Calculating gene and protein connections in a Parkinson's disease model
EurekAlert - FINDINGS: Researchers have created an algorithm that meshes existing data to produce a clearer step-by-step flow chart of how cells respond to stimuli. Using this new method, Whitehead Institute and Massachusetts Institute of Technology scientists have analyzed alpha-synuclein toxicity to identify genes and pathways that can affect cell survival. Misfolded copies of the alpha-synuclein protein in brain cells are a hallmark of Parkinson's disease.

RELEVANCE: Until now, data on gene expression and protein production have not been consistently analyzed together, leaving gaps in researchers' understanding of how various genes and proteins interact to form a cell's response to a stimulus. This new method could speed the development of therapies for a variety of diseases, including Parkinson's disease.
(information provided from the Northwest Parkinson Foundation newsletter)

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Rave Reviews in PD World! 

PBS Frontline - "My Father, My Brother, and Me," a personal documentary on Journalist Dave Iverson aired on tv Feb. 2, 2009.

You can view this program in its entirety by clicking this link:http://www.pbs.org/wgbh/pages/frontline/parkinsons/

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Massachusetts Institute of Technology 
News Release 29-Jan-2009
MIT IDs genes linked to Parkinson's side effects

CAMBRIDGE, Mass.--People with Parkinson's disease commonly suffer a slowing or freezing of movement caused by the death of neurons that make dopamine, a key chemical that allows brain cells to send and receive messages essential to voluntary movements. Patients regain the ability to move, seemingly miraculously, by taking L-DOPA or related drugs that mimic the missing dopamine. After a few years on L-DOPA, however, most patients again lose motor control — but in an opposite way. Instead of too little, there is too much movement, like involuntary nodding and rocking — side effects known as L-DOPA-induced dyskinesias.

"L-DOPA-induced dyskinesias are a major problem for patients, and there is a great need to help with these drug side effects," said MIT Institute Professor Ann Graybiel, a prominent Parkinson's researcher at the McGovern Institute for Brain Research at MIT.

Graybiel and her colleagues have identified two molecules whose expression in the brain is altered in the brains of animals with L-DOPA-induced dyskinesias. The results may lead to new approaches to the treatment of dyskinesias in Parkinson's patients, of which there are more than 1 million in the United States alone.

"We're very excited because these genes are concentrated in precisely the places that lose dopamine in Parkinson's disease, so they might be reasonable targets to go after therapeutically," Graybiel said. This research was published Jan. 26 in the advance online issue of Proceedings of the National Academy of Sciences.

The two related genes, named CalDAG-GEFI and CalDAG-GEFII, which are believed to be involved in signaling inside neurons, are expressed in the striatum, a brain structure essential for the control of movement and the main target of the dopamine-containing nerve tract that degenerates in Parkinson's disease.

In a rat model of Parkinson's disease, the two genes showed opposite changes when the animals were treated with L-DOPA. CalDAG-GEFI showed decreased expression while CalDAG-GEFII was increased.

"Moreover, the changes in the rat brain were proportional to the severity of the drug-induced dyskinesias. The more exaggerated the movements, the greater the dysregulation of these genes," said first author Jill Crittenden, a research scientist in the Graybiel Lab.

These CalDAG-GEF genes are thought to work by controlling the activity of other important signaling molecules (Ras, Rap and ERK) that are expressed in many different parts of the body and have many different biological functions. Other labs have shown that inhibiting Ras or ERK in animal models of dyskinesias prevents these involuntary movements.

"But because Ras and ERK do so many things, they are not promising drug targets because blocking them would probably have many unwanted effects," Crittenden said. "Because the CalDAG-GEF molecules control ERK and because they are so enriched in the very part of the brain that controls these involuntary movements, regulating them could have therapeutic value for dyskinesia without causing other problems." 

This study was funded by the Stanley H. and Sheila G. Sydney Fund, the National Institutes of Health, National Institute of Child Health and Human Development and the National Parkinson Foundation. Coauthors Ippolita Canturi-Castelvetri, Lauren Kett and Anne Young (Massachusetts General Hospital); Esen Saka (Hacettepe University, Turkey); Christine Keller-McGandy and Ledia Hernandez (MIT); and David Standaert (University of Alabama, Birmington) contributed to this study. Contact: Elizabeth Thomsonthomson@mit.edu617-258-5402

 

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Possibilities from the University of Nebraska Medical Center...
Brain Enzyme Could Lessen Impact Of Neurological Diseases
 
Jan. 16, 2009
OMAHA, Neb. - Researchers at the University of Nebraska Medical Center said they've found what may be a potentially lifesaving tool in the fight against brain diseases like epilepsy and dementia.
   "Whether it's epilepsy, dementia, stroke or Parkinson's, the essential problem is brain cells in particular regions die off," said neurologist Dr. Sanjay Singh.
   The UNMC researchers said they've discovered a naturally occurring enzyme, Peroxiredoxin 6, which could potentially reduce or even eliminate the effects of brain disease by preventing those cells from dying. Singh said his research partner was actually doing research on cataracts when he stumbled on the beneficial effects of the PRDX6 enzyme on brain cells.
   "We usually count cells to see how many survived and with this, it was visually apparent they were surviving," he said.       "The way it works is that it decreases oxidative stress. When you have a lot of oxidative stress in the brain, it kills brain cells."
   He said that since PRDX6 occurs naturally in the brain, the next step is figuring out how to increase its levels.
   "There are not very many neuroprotectors you can find that have been successful, so we'll have to start from scratch to choose our products and work on them," he said.
   He said if there's a way to increase the level of PRDX6, possibly through medication or diet, the impact could be life-changing.
   "Finding something like this is really exciting and gives us a brand new way of treating such disorders and gives hope to patients," he said.
   Doctors will need to test the enzyme in animal models before beginning human trials. They said right now, there's no known specific food or medication that will increase the enzyme in your body.
 Source: Parkinson's Information Exchange Network &msnbc

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Lack Of Vitamin D Linked To Parkinson's Disease
Science
Daily (Oct. 17, 2008) - A majority of Parkinson's disease patients
had insufficient levels of vitamin D in a new study from Emory University
School of Medicine.

The fraction of Parkinson's patients with vitamin D insufficiency, 55 percent, was significantly more than patients with Alzheimer's disease (41 percent) or healthy elderly people (36 percent).The finding adds to evidence that low vitamin D is associated with
Parkinson's, says first author Marian Evatt, MD, assistant professor of neurology at Emory. Evatt is assistant director of the Movement Disorders Program at Wesley Woods Hospital. The senior author is endocrinologist Vin Tangpricha, MD, assistant professor of medicine at Emory and director of the Endocrine Clinical Research Unit.Evatt says her team compared Parkinson's patients to Alzheimer's patients because they wanted to evaluate the possibility that neurodegenerative diseases in general lead to vitamin D insufficiency.

Most Americans get the majority of their vitamin D from exposure to sunlight or by dietary supplements; fortified foods such as milk and packaged cereals are a minor source. Only a few foods in nature contain substantial amounts of vitamin D, such as salmon and tuna.The body's ability to produce vitamin D using UV-B radiation from the sun decreases with age, making older individuals at increased risk of vitamin D deficiency. "We found that vitamin D insufficiency may have a unique association with Parkinson's, which is intriguing and warrants further investigation," Evatt

says.

The connection could come partly because patients with Parkinson's have mobility problems and are seldom exposed to the sun, or because low vitamin D levels are in some way related to the genesis or progression of the disease.She says her team saw their results as striking because their study group came from the Southeast, not a region with long gloomy winters, where vitamin D insufficiency is thought to be more of a problem. In addition, the study found that the fraction of patients with the lowest levels of vitamin D, described as vitamin D deficiency, was higher (23 percent) in the Parkinson's group than the Alzheimer's group (16 percent) or the healthy group (10 percent).

The retrospective study examined 100 people in each group, who were recruited between 1992 and 2007. Every fifth Parkinson's patient from Emory's clinical neurology database was selected, then healthy controls and patients with Alzheimer's disease were matched on age and state of residence.Vitamin D insufficiency is frequently defined as less than 30 nanograms per milliliter of blood of the 25-hydroxy form (the major storage form) of the vitamin and deficiency as less than 20 nanograms per milliliter. However,
most experts agree insufficiency warrants treatment and should not be
ignored.

Doctors have known for decades that vitamin D plays a role in bone formation, Evatt says. More recently, scientists have been uncovering its effects elsewhere, including producing peptides that fight microbes in the skin, regulating blood pressure and insulin levels, and maintaining the nervous system. Low vitamin D levels also appear to increase the risk of several cancers and auto-immune diseases such as multiple sclerosis and diabetes.

Previous studies have shown that the part of the brain affected most by Parkinson's, the substantia nigra, has high levels of the vitamin D receptor, which suggests vitamin D may be important for normal functions of these cells, Evatt says.Emory clinicians are conducting further research to investigate whether vitamin D insufficiency is a cause or possibly a result of having Parkinson's. In a pilot study, Parkinson's patients are receiving either standard or larger doses of vitamin D, with an eye towards possibly reducing
the severity of their condition.The research was funded by the National Center for Research Resources, the
National Institute of Aging and the National Institute of Environmental Health Sciences of the National Institutes of Health, and by an anonymous donor.  

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MICHAEL J FOX  MOVES FAST TO ADVANCE PARKINSON'S APPLICATION OF FDA-APPROVED DIABETES DRUG

Marina Emborg, MD, PhD, of the University of Wisconsin, Madison, has received supplemental funding from MJFF to advance her study of the FDA-approved diabetes drug pioglitazone as a potentiallyneuroprotective treatment for Parkinson's disease.

Because of its documented anti-inflammatory and anti-oxidative stress properties, Dr. Emborg hypothesized that it might hold potential to rescue dopamine neurons from death. Dr. Emborg was funded by MJFF to test pioglitazone's neuroprotective effects in pre-clinical models of PD. Encouragingly, her results confirmed her hypothesis. Most recently, when pre-clinical models received oral pioglitazone at a dose equivalent to that used to treat diabetic patients, the treatment induced benefits observable in the models' function and in
pathological studies.

Pioglitazone is already FDA-approved for use in humans. With promising pre-clinical results in Parkinson's, it could quickly advance to
clinical trials in patients. MJFF has quickly funded Dr. Emborg to take the next steps toward a potential clinical trial. She is now
working to assess how much pioglitazone is present in cerebrospinal fluid after it's taken orally. The results will help understand how
much pioglitazone is needed to induce neuroprotection, data critical to optimize dosing in a clinical trial.

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Pain is common in PD

Unlocking mysteries......
Dopamine reshapes key brain circuits that control behavior
CHICAGO -- Parkinson's disease and drug addiction are polar opposite diseases, but both depend upon dopamine in the brain. Parkinson's patients don't have enough of it; drug addicts get too much of it. Although the importance of dopamine in these disorders has been well known, the way it works has been a mystery.
   New research from Northwestern University's Feinberg School of Medicine has revealed that dopamine strengthens and weakens the two primary circuits in the brain that control our behavior. This provides new insight into why a flood of dopamine can lead to compulsive, addictive behavior and too little dopamaine can leave Parkinson's patients frozen and unable to move.
   "The study shows how dopamine shapes the two main circuits of the brain that control how we choose to act and what happens in these disease states, " said D. James Surmeier, lead author and the Nathan Smith Davis Professor and chair of physiology at the Feinberg School. The paper is published in the August 8 issue of the journal Science.
   These two main brain circuits help us decide whether to act out a desire or not. For example, do you get off the couch and drive to the store for an icy six-pack of beer on a hot summer night, or just lay on the couch? One circuit is a "stop" circuit that prevents you from acting on a desire; the other is a "go" circuit that provokes you to action. These circuits are located in the striatum, the region of the brain that translates thoughts into actions.
   In the study, researchers examined the strength of synapses connecting the cerebral cortex, the region of the brain involved in perceptions, feelings and thought, to the striatum, home of the stop and go circuits that select or prevent action. Scientists electrically activated the cortical fibers to simulate movement commands and boosted the natural level of dopamine. What happened next
surprised them. The cortical synapses connecting to the "go" circuit became stronger and more powerful. At the same time, dopamine weakened the cortical connections in the "stop" circuit.
   "This could be what underlies addiction," Surmeier said. "Dopamine released by drugs leads to abnormal strengthening of the cortical synapses driving the striatal 'go' circuits, while weakening synapses at opposing 'stop' circuits. As a result, when events associated with drug taking – where you took the drug, what you were feeling – occur, there is an uncontrollable drive to go and seek drugs."
   "All of our actions in a healthy brain are balanced by the urge to do something and the urge to stop," Surmeier said. "Our work suggests that it is not just the strengthening of the brain circuits helping select actions that is critical to dopamine's effects, it is the weakening of the connections that enable us to stop as well. "
   In the second part of the experiment, scientists created an animal model of Parkinson's disease by killing dopamine neurons. Then they looked at what happened when they simulated cortical commands to move. The result: the connections in the "stop" circuit were strengthened, and the connections in the "go" circuit were weakened.
   "The study illuminates why Parkinson's patients have trouble performing everyday tasks like reaching across a table to pick up a glass of water when they are thirsty," Surmeier said. Surmeier explained the phenomenon using the analogy of a car. "Our study
suggests that the inability to move in Parkinson's disease is not a passive process like a car running out of gas," he said. "Rather, the car doesn't' move because your foot is jammed down on the brake. Dopamine normally helps you adjust the pressure on the brake and gas pedals. It helps you learn that when you see a red light at an intersection, you brake and when the green light comes on, you take your foot off the brake and depress the gas pedal to go. Parkinson's disease patients, who have lost the neurons that release
dopamine, have their foot perpetually stuck on the brake."
   Understanding the basis for these changes in brain circuitry moves scientists closer to new therapeutic strategies for controlling these brain disorders and other involving dopamine like schizophrenia, Tourette's syndrome and sdystonia.
 

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 Some Personal PD Stories

(The following is provided by our friends at the Northwest Parkinson' s Foundation...and their bi-monthly "Parkinson's Post")

A City of Strangers and Kindness

The New York Times - I can spot Marty in a crowd a block away. He tilts left into the wind, as if he were shouldering the full blast of Hurricane Katrina, his arm gesticulating awkwardly. Once a well-dressed woman asked if I had seen “that man — I think he’s drunk.” I assured her the man was my husband. “He has Parkinson’s,” I told her.

We get that a lot — snickers, whispers. Looks that wound. “When people stare,” Marty tells me, “I get nervous and shake that much more.”

There are no rules of etiquette for dealing with a person who has a neurological disorder. Some people do stare; others recoil. Fortunately, though, many are genuine and forthcoming in their help. And that is as true here in New York City, supposedly the capital of heartless impatience, as it is anywhere in the country.

Marty has to take a combination of seven drugs eight times a day. He bought an expensive pillbox specifically made for Parkinson’s patients; an alarm goes off when it’s time to take a pill. One problem: the container is so difficult to open that when he finally succeeds, the pill is likely to go flying across the room or, worse, into the street.

Even when he’s able to grasp the pill and take it, it may not last as long as he would like. “After a few years of taking medication, people with Parkinson’s may begin to experience ‘wearing off’ spells,” Dr. Lawrence I. Golbe, a neurologist at Robert Wood Johnson University Hospital in New Brunswick, N.J., recently wrote in the Parkinson’s Disease Foundation newsletter, adding that for some patients the drugs may be effective for only three hours.

At home it’s a minor inconvenience, though worrisome. Outside it’s a potential disaster. Sometimes Marty’s upper body moves but his feet stick, and he falls. Once a sergeant called from Penn Station. He said Mr. Sternberg was resting, just shaken up a little. “We’ll send him home as soon as he’s able,” he said. Bless those men and women in blue.

One afternoon a young woman saw Marty leaning unsteadily against a street pole. She insisted on helping him. He insisted she didn’t. She finally grabbed his arm, hailed a taxi and delivered him to our doorman, two blocks away. “Merry Christmas,” she said with a smile.

A week later his pills gave out in front of Grand Central Terminal.

“Want to put a shine on those shoes?” an old-timer beckoned. It was sleeting; Marty was shaking. (Cold weather aggravates his tremor.) Did he need anything to drink or eat?

“Just some water for my pills. Thanks.”

Why was he out on such a day? Marty showed him two simple gold wedding bands he had just bought for our 20th anniversary.

“It’s a surprise for my wife,” he said. “I could never wear a ring; my fingers were too thick. Now it seems I can.”

Experts do say that Parkinson’s patients burn more calories than other people. “If there’s any consolation to this disease,” Marty said, “it’s that I can indulge in Ben & Jerry’s Chocolate Fudge Brownie without guilt.”

I have a sign taped on the inside of our front door listing vital items: pills, wallet, phone. Sometimes he forgets to look. The other day a saleswoman at Radio Shack tried to help a flustered Marty find his wallet.

“I know it was here,” he said. “Maybe I dropped it on the street looking for my pills.”

Before she could calm him down, he left under a black sky ready to burst with rain. Was it in the trash? No luck. We searched the apartment; it was on the closet floor. Perhaps we should have a sign reminding us to look at the sign.

The following morning he returned to Radio Shack. The saleswoman asked if he had found his wallet. He sheepishly admitted it had never left the apartment.

“Oh, yes,” she said. “I prayed to St. Anthony for you, the patron saint of lost articles. He must have heard me.”

I know I can be guilty of treating Marty like a child; impatience gets the better of me. “Hold on to the railing, pick your feet up so you don’t trip, don’t run for the bus. Be careful.” These admonitions are taken with a grain of salt; after all, he is 13 years my senior.

“Don’t make mountains out of molehills,” he constantly reassures me.

Still, I hold my breath whenever he ventures out. But perhaps a little less these days — my fears of the city tempered by the grace and good will of its people.

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  Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional.

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