Parkinson's Disease Support Group

It's Time to Take Action!

GO TO LINK AT BOTTOM; this is so easy; takes 2 min. tops!

Call Now

Enter Your Zip Code

bettyg note: if your sen. is NOT on this committee, when you enter the zip code; i believe it will show something to that effect.

in my case, CHAIR TOM HARKIN, is from iowa; i entered my zip code and his name popped up with ALL info, phone no. and they have the brief speech there too.

so when i called in on parkinson's, I ADDED CHRONIC LYME DISEASE to my requet for both illnesses!

THANKS TO YOU WHOSE SENATORS ARE ON THIS COMMITTEE!!

Important federal budget decisions for FY 2013 are being made right now. Call your Senator today and ask him or her to make funding increases for biomedical research a top priority!

On Tuesday, the U.S. Senate Appropriations Subcommittee on Labor, Health and Human Services, Education, and Related Agencies (L-HHS) will vote on the NIH FY13 budget.

MY IOWA Senator sits on this Committee and we need you to call today and tell him or her that their support for this research is critical to the between 500,000 and 1.5 million Americans living with Parkinson's.

CALL YOUR SENATOR NOW!

http://www.capwiz.com/pan/callalert/index.tt? alertid=61450501

bettyg, iowa activst PARKINSON/LYME DISEASE

June 14, 2012

The following is a statement from Parkinson's Action Network CEO Amy Comstock Rick:

"Today, the U.S. Senate Appropriations Committee, which oversees funding for the National Institutes of Health (NIH), recommended only a modest budget increase instead of funding the NIH at a level which would allow it to keep pace with inflation, encourage innovation, and strengthen local economies in the cities and towns across America where NIH-funded research happens.

The biomedical research and patient advocacy communities came together to recommend Congress and the president fund the NIH at a minimum of $32 billion for Fiscal Year 2013. While we appreciate the modest increase the Senate committee provided, it is not enough.

"A Fiscal Year (FY) 2013 funding level of $30.723 billion--an increase of $100 million above FY 2012--will not allow the NIH to remain a global leader in research and development.

NIH funding over the past nine years has not come close to meeting the rate of inflation, putting at risk biomedical research innovation and taxpayers' health and well-being.

Federal investment in biomedical research not only helps encourage private sector growth and investment, it also strengthens our nation's long-term health.

As our population ages, more people will be diagnosed with diseases like Parkinson's, and without strong federal investment in the fight for better treatments and cures, the burden only worsens.

"On behalf of the Parkinson's community, we call on Congress to take a good hard look at how investments in NIH can have a broader impact across the country and around the world, and fund the NIH at the highest level."

*****

fyi, tomorrow i'll be gone all day at annual parkinson's conference in des moines; what a TIRING day sitting and driving 2 hrs. RT.

bettyg, iowa PARKINSON'S/LYME ACTIVIST

Some patients experience a 'sleep benefit' after daytime naps and nighttime shuteye

By Mary Elizabeth Dallas

Friday, June 22, 2012

FRIDAY, June 22 (HealthDay News) --

Sleep seems to improve the motor function of people with Parkinson's disease, researchers have found.

This "sleep benefit" occurs for some patients even though they are without their medication while sleeping, the study authors said.

However, how sleep helps patients' motor function remains unclear, and not all Parkinson's patients experience this improvement, according to the report, published in the June issue of the Journal of Parkinson's Disease.

"If the subjective experience of sleep benefit is proven to be related to an objective improvement in motor function, this could have considerable clinical benefits," the study's lead investigator Dr. Sebastiaan Overeem, of the department of neurology, Donders Institute for Brain, Cognition and Behavior at Radboud University Nijmegen Medical Centre in the Netherlands, said in a journal news release.

In conducting the study, the researchers questioned 243 patients with Parkinson's disease about their motor and non-motor symptoms. They also assessed the patients' symptoms of depression, functioning and quality of life.

The investigators found that nearly 47 percent of the patients experienced a sleep benefit, or a clear improvement in their Parkinson's symptoms after a night's sleep.

Daytime naps were also taken by 98 of the 243 patients. Of these "regular nappers," 46 percent did not notice a sleep benefit at all.

On the other hand, 20 percent of nappers said they experienced a reduction in their Parkinson's symptoms only after a night of sleeping, and 13 percent reported an improvement only after their nap.

Meanwhile, 20 percent of nappers reported an improvement in their symptoms following both their naps and nighttime sleep.

"It is tempting to speculate whether daytime naps might constitute a possible therapeutic application," noted Overeem.

While the study uncovered an association between sleep and Parkinson's symptoms, it did not prove a cause-and-effect relationship.

The researchers pointed out that there were no demographic or clinical differences -- such as age at onset of the disease and type of treatment -- between those who experienced the sleep benefit and those who did not.

There were also no differences in depression, quality of life, memory, fatigue and sleep quality between these two groups.

The study authors added that their findings are based on patients' perceptions of a sleep benefit, which are subjective.

More research is needed to objectively assess changes in symptoms of Parkinson's disease after a period of sleep.

"Further study is important to identify possible determinants and underlying mechanisms of sleep benefit, in order to identify those patients most likely to benefit from sleep," Overeem concluded.

"Both our research and previous studies show it's important to renew research on this intriguing subject."

SOURCE: Journal of Parkinson's Disease, news release, June 20, 2012

http://www.nlm.nih.gov/medlineplus/news/ fullstory_126561.html

Copyright (c) 2012 HealthDay. All rights reserved.

By Nancy Walsh, Staff Writer, MedPage Today

Published: June 27, 2012

Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and Dorothy Caputo, MA, BSN, RN, Nurse Planner

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Action Points

REM sleep behavior disorder, a rare condition, appears to share some risk factor associations such as occupational pesticide exposure with Parkinson's disease.

Note, however, that smoking, which appears protective for Parkinson's disease, was more prevalent for REM disorder cases over controls in this study.

A rare sleep disorder characterized by disturbances of rapid eye movement (REM) sleep shares some environmental risk factors with Parkinson's disease, an international case-control study suggested.

For example, occupational pesticide exposure has been clearly linked with Parkinson's disease, and in this study patients with REM sleep behavior disorder were twice as likely to have been exposed to pesticides as controls (OR 2.23, P=0.008), according to Ronald B. Postuma, MD, of McGill University in Montreal, and colleagues.

But other environmental risk factors common to Parkinson's disease do not come in to play in the sleep disorder.

For instance, patients who don't drink coffee have consistently been shown to be at higher risk for Parkinson's disease, but no such association was found in patients with the REM sleep disorder (OR 0.95, 95% CI 0.59 to 1.47), the researchers reported online in the July 31 issue of Neurology.

REM sleep behavior disorder is characterized by the absence of muscle atonia usually present during REM sleep and by "dream enactment," during which disruptive and aggressive behaviors can occur.

The condition has been linked with the later development of Parkinson's disease and Lewy body dementia, and may be a preclinical sign or a specific subtype.

"Idiopathic [REM sleep behavior disorder] as a syndrome has an unusual status -- it exists both as an independent sleep condition and as a prediagnostic marker of synuclein-mediated neurodegenerative disease," Postuma and colleagues explained.

Because of the rarity of the disorder -- the prevalence has been estimated to be 0.4% to 0.5% in adults -- little has been known about risk factors.

So the international REM Sleep Behavior Disorder Study Group has combined the patient populations from 13 centers in 10 countries, and Postuma and colleagues have analyzed behavioral and exposure risk factors for 347 patients with the disorder.

A control group consisted of 218 patients with other sleep disorders and 129 healthy volunteers, matched for age and sex.

Mean age of the cases was 68 years and 81% were men.

Overall, factors that were associated with the REM sleep disorder were pesticide exposure, cigarette smoking, head injury, lower educational achievement, and working on a farm.

Unlike Parkinson's disease, where nonsmokers typically have been considered at greater risk for the disorder, in this analysis patients who had ever smoked cigarettes had an increased risk for the REM sleep disorder compared with controls (OR 1.43, 95% CI 1.04 to 1.98).

Current cigarette smokers also were at elevated risk (OR 1.45, 95% CI 0.84 to 2.50).

"One of the most intriguing aspects of this work is the picture of similarities and differences among risk factors," observed Christian Guilleminault, MD, of Stanford University in Palo Alto, Calif., and colleagues.

"While pesticide exposure appears to be a risk factor for both disorders, smoking, for example, which is protective for [Parkinson's disease], is a risk factor for [REM sleep behavior disorder]," Guilleminault's group wrote in an accompanying editorial.

Patients with the REM disorder were more likely to have experienced a head injury with loss of consciousness (OR 1.59, 95% CI 1.03 to 2.46, P=0.037).

Additional factors associated with the sleep disorder included the number of years of schooling (11.1 years versus 12.7 years, P<0.001), and farming as an occupation (OR 1.67, P=0.022).

Other types of jobs such as mining and teaching were not associated with the disorder, while a borderline relationship was seen for welding (OR 1.53, P=0.063).

In a sensitivity analysis, the association between certain factors such as smoking, head injury, and farming and the REM disorder was stronger when affected patients were compared with healthy controls than when they were compared with patients who had other sleep disorders. That may have been related to the "healthy volunteer effect," in which people who volunteer to participate in research may be more health-conscious in general, the authors noted.

However, overmatching with controls who have other sleep disorders could have occurred if they shared risk factors with the REM disorder, the investigators also noted.

Limitations included the cross-sectional design of the study and the possibility of recall bias, particularly for patients who may have preclinical dementia.

There also may be differences in patients with REM sleep behavior disorder who are referred to specialty clinics and those who are never seen at such centers, so a population-based study could provide additional useful information, the researchers noted.

The study was funded by the Fonds de la Recherche en Sante du Quebec.

The authors reported no financial disclosures.

Primary source: Neurology

Source reference:

Postuma R, et al "Environmental risk factors for REM sleep behavior disorder: a multicenter case-control study" Neurology 2012;

Additional source: Neurology

Source reference:

Sullivan S, et al "Hiding in plain sight: risk factors for RE sleep behavior disorder" Neurology 2012;

http://www.medpagetoday.com/Neurology/SleepDisorders/33513? utm_content=&utm_medium=email&utm_campaign=DailyHeadlines&utm_source=

© 2012 Everyday Health, Inc. All rights

(10 votes)

By K Kimberly McCleary • ProHealth.com • June 27, 2012

This article on the many faces of orthostatic intolerance (problems with heart rate & blood pressure control, common in ME/CFS and fibromyalgia) was published June 19, 2012 on the CFIDS Association's Research1st Blog (www.Research1st.com).

It is reproduced here with kind permission. ©2012 CFIDS Association of America. All Rights Reserved.

___________________________________

The Outs and Ins of OI, Orthostatic Intolerance

June 19, 2012

By K. Kimberly McCleary, President & CEO,

CFIDS Association of America

On Friday [June 18] we posted a link to an article in TIME magazine’s Healthland section, “Tip for Insomniacs: Cool Your Head to Fall Asleep,” on our Facebook page - https://www.facebook.com/CFIDSAssn.

“When Buysse’s group [at University of Pittsburgh] gave 12 insomniacs a cap to wear that contained circulating water at cool temperatures, they were able to get them to fall asleep almost as easily as people without sleep disorders:

• Using the caps, the insomniacs took about 13 minutes to fall asleep, compared with 16 minutes for the healthy controls,

• And they slept for 89% of the time they were in bed, which was similar to the amount of time the controls spent asleep.”

The comments posted in response to the article were split between readers who expressed problems with sleep (common in CFS) and readers who found different temperatures to affect their symptoms (also common in CFS). Of those who commented about temperature, most had trouble in warm environments.

While many people with CFS are knowledgeable about a condition called “orthostatic intolerance” (OI) that often co-occurs with CFS, every time we post something about OI, we hear from at least one person who wasn’t aware of it, but reports that it explains a lot of the “weird” symptoms they experience.

With summer heat on its way, and because treatment of OI through medication, dietary and postural approaches can provide symptom relief, it can be an important part of managing CFS - especially when temperatures rise.

Some Basics

OI is the development of a set of characteristic symptoms while standing or sitting upright.

It has been associated with CFS in both adults and children.

The 1986 definition of myalgic encephalomyelitis (M.E.) by Melvin A. Ramsey, MD, includes “orthostatic tachycardia” as one of the accompanying features.

The first research study connecting OI and CFS was published in the Lancet in 1995, by Peter Rowe, MD, and associates at Johns Hopkins University, who identified a type of OI called neurally mediated hypotension (NMH) in CFS patients.

Since 1995, scientists have learned much more about the broader problem of OI in CFS.

It is now thought that many CFS patients (up to 97% in some studies) have some form of OI and it seems to be a particular problem in young people with CFS.

Dr. Rowe presented a webinar about OI and its management on Sept. 1, 2010, as part of the Association’s 2010 Webinar Series. The recording and his slides provide an excellent overview.

He also shared his clinic’s written material about OI and medications, postural and dietary complements to comprehensive management of OI.

Types of OI

There are many types of OI. When you round up experts who study the autonomic nervous system (as we did at one of our research symposia in the year 2000), they have trouble agreeing on the names and definitions for the various types of OI. (Does that sound familiar?)

• OI and other forms of dysautonomia are common in other conditions like MS and Parkinson’s;

• It also occurs in less well-studied conditions like Ehler’s Danlos Syndrome, Marfan syndrome and Shy-Drager Syndrome.

So, it’s not unique to or diagnostic of CFS.

At least two specific forms of OI have been linked with CFS in multiple research studies:

Neurally mediated hypotension (NMH) and postural orthostatic tachycardia syndrome (POTS):

• NMH is a precipitous drop (at least 20-25 mm Hg) in systolic blood pressure when standing. The blood pressure drop is accompanied or preceded by an increase in symptoms.

• POTS is a rapid increase in heart rate (pulse) of more than 30 beats per minute (bpm) from baseline, or to more than 120 bpm total, during the first 10 minutes of standing.

It is also known as chronic orthostatic intolerance, or COI.

OI is easier to recognize (and treat) in individuals who have normal or low resting blood pressure.

But it’s also possible for OI to be a problem for people who have high blood pressure.

As you can see from the description above, forms of OI describe blood pressure control and heart rate control problems that are provoked by upright posture.

Symptoms of OI

The blood pressure and heart rate changes in NMH and POTS are accompanied by orthostatic symptoms such as

lightheadedness, dizziness, nausea, fatigue, tremors, breathing or swallowing difficulties, headache, visual disturbances, sweating and pallor.

Many patients develop swollen, bluish legs, providing evidence of blood pooling in the lower part of the body.

These symptoms can become worse or be provoked more quickly in warm temperatures or hot indoor environments like saunas.

(This last part is what many people who commented on the cooling cap story reported.)

OI should be better understood by primary doctors than it probably is, but if you suspect you might have OI, start there.

You may have to see a specialist for a formal evaluation.

Expect an extra challenge from your doctor(s) if you haven’t ever fainted; many doctors only associate OI with forms that involve “syncope” or fainting.

You can learn more about testing for and the underlying pathophysiology of OI here. [See also Dr. David Bell's description of his orthostatic testing procedure here.]

(Update: For more specific information about the possible confusion between symptoms of OI and anxiety prompted by a question arising from this post. Please see my post, “Is It Anxiety or OI?”)

OI Treatment

Effective treatment for NMH and POTS in CFS must be individualized.

In general, treatment for POTS and NMH helps greatly to alleviate some symptoms, but rarely fully resolves the CFS. For some people, it makes a huge difference.

According to the experts, the first line of treatment should be non-medical interventions, such as:

• Increasing fluids and salt,

• Tilting the head of the bed up a few degrees,

• Wearing compression garments (such as support hose, girdles or abdominal binders),

• And learning to avoid and cope with things that can make OI worse (such as standing in long lines, being in warm environments and eating large, heavy meals).

Here are some of the top “tips” for managing OI compiled from various articles and our readers: http://www.cfids.org/cfidslink/2009/070105.asp

If these are not effective, doctors may introduce pharmaceutical treatments such as:

• Fludrocortisone (Florinef) to treat low blood volume;

• And vasoconstrictor medications, including methylphenidate (Ritalin), dextroamphetamine (Dexedrine) and midodrine (ProAmatine) to treat blood pooling (Inderal or Tenormin);

• And sometimes drugs to block the release or effect of epinephrine and norepinephrine.

Selective serotonin reuptake inhibitors (SSRIs) have been used with some success in patients with POTS, and one randomized trial has demonstrated the efficacy of paroxetine (Paxil) for those with recurrent syncope due to NMH.

Intravenous saline can help reduce symptoms, especially following HUT or other acute exacerbations of symptoms.

Common syncope treatments beta-blockers and clonidine may be less effective in POTS and may reflect different causes for POTS and simple fainting. You can learn more about the medications used to treat OI.

OI and its connection to CFS remains a vigorous area of research and the CFIDS Association has supported several studies looking at different mechanisms for the autonomic nervous system problems that are common in CFS.

You can hear Dr. Marvin Medow of New York Medical College describe his Association-funded study on our webinar, Going With the Flow. You can also... search Research1st.com using the tags autonomic nervous system, NMH, orthostatic intolerance, POTS, or treatment for other articles about orthostatic intolerance.

Like CFS itself, managing OI generally requires a combination of pharmacological and non-pharmacological therapies.

Small changes can have positive effects over time, especially if they become routine. Whether it’s a cooling cap or finding the right beta blocker, it may be worth exploring.

K. Kimberly McCleary has served as the Association’s chief staff executive since 1991.

(Updated by the author on June 20, 2011.)

____

Disclaimer: These statements not been evaluated by the FDA.

They are generic and are not intended to prevent, diagnose, treat or cure any condition, illness or disease; nor are they meant to replace professional medical advice, diagnosis and treatment.

It is very important that you make no change in your healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.

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Post edited by: Bettyg, at: 07/03/2012 12

Wednesday, July 4, 2012 - 2 p.m. EDT

Contact: Daniel Stimson, NINDS 301-496-5751

NIH-funded study shows cells from different patients have unique drug responses

Researchers have taken a step toward personalized medicine for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments. The study was funded by the National Institutes of Health.

The researchers collected skin cells from patients with genetically inherited forms of Parkinson’s and reprogrammed those cells into neurons.

They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability — in particular, abnormalities in the cellular energy factories known as mitochondria.

At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.

The results were published in Science Translational Medicine.

"These findings suggest new opportunities for clinical trials of Parkinson’s disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).

A consortium of researchers conducted the study with primary funding from NINDS. The consortium is led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston.

The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells.

The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.

Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra.

There, it destroys neurons that produce the chemical dopamine.

Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms.

Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.

Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role.

There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease.

Researchers have also identified nine genes that, when mutated, can cause the disease.

Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease.

By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses.

Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1.

The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.

Because prior studies have suggested that Parkinson's disease involves a breakdown of mitochondrial function, the researchers looked for signs of impaired mitochondria in patient-derived neurons.

Mitochondria turn oxygen and glucose into cellular energy.

The researchers found that oxygen consumption rates were lower in patient cells with LRRK2 mutations, and higher in cells with the PINK1 mutation.

In PINK1 mutant cells, the researchers also found increased vulnerability to oxidative stress, a damaging process that in theory can be counteracted with antioxidants.

Next, the researchers tested if neurons derived from patients and healthy volunteers were vulnerable to a variety of toxins, including some that target mitochondria.

Compared to neurons from healthy individuals, patient-derived neurons were more likely to become damaged or die after exposure to mitochondrial toxins.

Patient-derived neurons also suffered more damage from the toxins than did patient-derived skin cells.

Next, the researchers attempted to rescue the toxin-exposed cells with various drug treatments that have shown promise in animal models of Parkinson's, including the antioxidant coenzyme Q10 and the immunosuppressant rapamycin.

All patient-derived neurons — whether they carried LRRK2 or PINK1 mutations — had beneficial responses to coenzyme Q10.

However, the patient-derived neurons differed in their response to rapamycin; the drug helped prevent damage to neurons with LRRK2 mutations, but it did not protect the neurons with PINK1 mutations.

This cluster of human iPS cells has been induced to express neural proteins, which have been tagged with fluorescent antibodies. Courtesy of Dr. Ole Isacson, McLean Hospital and Harvard Medical School.

These results hint that iPS cell technology could be used to help define subgroups of patients for clinical trials.

To date, interventional trials for Parkinson's disease have not focused on specific groups of patients or forms of the disease, because there have been few clues to point investigators toward individualized treatments.

Although the current study focused on genetic forms of Parkinson's, iPS cell technology could be used to define disease mechanisms and the most promising treatments for sporadic Parkinson's as well.

The NINDS Parkinson's Disease iPS Cell Research Consortium is one of three such consortia funded by NINDS.

One of the consortia is focused on developing iPS cells for the study of Huntington's disease, and another focuses on amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.

The Huntington's disease consortium recently reported successful derivation of iPS cells and iPS-generated neurons from patients.

Cells from patients with both early and later onset disease showed severe defects in physiology, metabolism, and cell viability, compared to cells from healthy volunteers.

These results were reported in the June 28th issue of Cell Stem Cell.

The consortium is led by led by Leslie Thompson, PhD, a professor of psychiatry and human behavior at the University of California, Irvine.

Skin cell and iPS cell lines developed by the consortia are available to both academic and industry researchers through the NINDS human cell line repository at the Coriell Institute.

To date the NINDS repository has distributed more than 200 cell lines worldwide.

The Parkinson's Disease iPS Cell Research Consortium is funded primarily by grants and contracts from NINDS (NS070276, NS078338).

The three disease consortia were started in 2009 with more than $11 million in NINDS grants, made possible by the Recovery Act.

Funding for the consortia was recently renewed through 2013 via a public-private partnership.

Future goals include increasing the number of iPS cell lines and the variety of mutations represented, and giving some lines biological tags that will enable researchers to see when the cells have transformed into specific neuronal types.

NINDS is funding this next phase in collaboration with the Michael J. Fox Foundation, the Parkinson's Disease Foundation, the ALS Association, the Association for Frontotemporal Degeneration, the CHDI Foundation, the Huntington's Disease Society of America, the Hereditary Disease Foundation, and the California Institute for Regenerative Medicine.

For more information about Parkinson's disease, visit http://www.ninds.nih.gov/disorders/parkinsons_disease/ parkinsons_disease.htm.

NINDS (http://www.ninds.nih.gov) is the nation's leading funder of research on the brain and nervous system.

The NINDS mission is to reduce the burden of neurological disease – a burden borne by every age group, by every segment of society, by people all over the world.

About the National Institutes of Health (NIH):

NIH,the nation's medical research agency,includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services.

NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research,and is investigating the causes, treatments, and cures for both common and rare diseases.

For more information about NIH and its programs, visit http://www.nih.gov.

About the National Institutes of Health (NIH):

NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services.

NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases.

For more information about NIH and its programs, visit www.nih.gov.

NIH...Turning Discovery Into Health

References:

Cooper, Oliver and Seo, Hyemyung et al. for the NINDS Parkinson's Disease iPS Cell Research Consortium. "Familial Parkinson’s disease iPSCs show cellular deficits in mitochondrial responses that can be pharmacologically rescued." Science Translational Medicine, published online July 4, 2012. DOI: 10.1126/scitranslmed.3003985

Mattis, Virginia et al. for the NINDS Huntington's Disease iPS Cell Consortium. "Induced pluripotent stem cells from patients with Huntington’s disease show CAG repeat expansion associated phenotypes." Cell Stem Cell, published online June 28, 2012. DOI: 10.1016/j.stem.2012.04.027

http://www.nih.gov/news/health/jul2012/ninds-04.htm

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Physical abilities, quality of life start to deteriorate up to 7 years earlier, study says

By Mary Elizabeth Dallas

Friday, July 6, 2012

FRIDAY, July 6 (HealthDay News) --

Parkinson's disease patients experience declines in physical abilities and quality of life several years before the degenerative disease is diagnosed, new research finds.

In women, the declines started about 7.5 years before diagnosis, while in men, declines were noted at three years prior to diagnosis, according to the study in the June 2 issue of the Journal of Parkinson's Disease.

Parkinson's disease occurs when the neurons that produce dopamine, a crucial brain chemical, in certain regions of the brain die.

Symptoms, which worsen over time, can include tremors, stiffness, slurred speech and trouble walking.

Researchers examined information on 51,000 men enrolled in the Health Professionals Follow Up Study and 122,000 women enrolled in the Nurses' Health Study.

The men completed questionnaires about their health-related quality of life, including physical functioning, limitations due to physical and emotional problems, mental health issues and pain.

The women answered questions about their physical functioning.

Researchers identified 454 men and 414 women with Parkinson's disease.

Until about 7.5 years before diagnosis, physical function for both men and women was similar to that of men and women who were not later diagnosed with Parkinson's.

From this point on, however, women with the disease began to experience a decline in their physical function, while men's decline in physical function and well-being began around three years prior to diagnosis.

"We observed a decline in physical function in [Parkinson's disease] patients relative to their healthy counterparts beginning three years prior to diagnosis in men and seven and a half years prior to diagnosis in women," study lead investigator Natalia Palacios, of Harvard School of Public Health, said in a journal news release.

"The decline continues at a rate that is five to seven times faster than the average yearly decline caused by normal aging in individuals without the disease."

Researchers said the study suggests that the Parkinson's disease process may start years before symptoms become obvious.

"This result provides support to the notion that the pathological process leading to PD [Parkinson's disease] may start several years before PD diagnosis," Palacios concluded.

"Our hope is that, with future research, biological markers of the disease process may be recognizable in this preclinical phase."

SOURCE: Journal of Parkinson's Disease, news release, July 2, 2012

http://www.nlm.nih.gov/medlineplus/news/ fullstory_127008.html

Copyright (c) 2012 HealthDay. All rights reserved.

Symptoms include tremor, rigidity, extreme slowness of movement, and impaired balance.

Swallowing and speaking difficulties are also common, as are several non-motor symptoms that seriously affect quality of life.

YESTERDAY

Basic research on chemical signals in the brain, called neurotransmitters, led to recognition that the symptoms of PD reflect loss of nerve cells that normally release the neurotransmitter dopamine.

Recognition of the loss of dopamine cells in PD led to development of the drug levodopa, which nerve cells turn into dopamine. Levodopa dramatically reversed symptoms of PD for several years in many people.

Levodopa, however, did not slow the underlying neurodegeneration and became less effective as PD progressed.

Levodopa also induced side effects including uncontrolled movements, called dyskinesias, and “on-off” fluctuations in symptom control.

Brain surgery that permanently destroyed regions of tissue involved in PD provided some benefit for people with the disease. This was the only validated non-drug therapy available at that time.

Neurosurgeons also transplanted fetal tissue, adrenal tissue, and other cells that might produce dopamine into the brains of people with PD.

The safety and effectiveness of these procedures were controversial.

With the exception of a few PD-like disorders associated with viral infections, certain toxins, and a “punch drunk” syndrome exhibited by aging boxers, the origins of PD were mysterious.

TODAY

Although estimates vary, about 50,000 people are diagnosed with PD in the U.S. each year and about half a million people have the disease. Because the rate of PD increases in older adults, the burden will increase unless prevention and treatment improve.

Levodopa is still the mainstay of drug therapy.

Several additional drugs are now available that complement levodopa therapy, but none significantly slows the underlying neurodegeneration.

Discoveries about how the brain controls movement and improved technology led to Deep Brain Stimulation (DBS).

DBS improves symptoms of PD by electrically stimulating brain cells in movement control areas of the brain through chronically implanted electrodes.

A joint Veterans Administration –NIH clinical trial confirmed the benefits of DBS for advanced PD, and efforts to improve DBS are ongoing.

Two NIH-supported clinical trials of fetal tissue transplantation demonstrated that this approach to treating PD is problematic, causing serious dyskinesias.

However, results also provided encouragement for better controlled methods of cell transplant therapy.

Research has identified several genes that can cause rare inherited forms of PD and other genes that influence age of onset and susceptibility to common PD.

Ever more powerful gene discovery methods, including Genome Wide Association Studies and Deep Sequencing, are now revealing more genetic contributions to PD.

Gene findings are yielding clues about what kills brain cells in inherited and non-inherited PD and suggesting new strategies, now at various stages of testing, to slow the course of disease.

Several studies suggest environmental influences on PD.

Exposure to certain pesticides may increase risk, and higher intake of vitamin D, caffeine, and tobacco may be associated with lower incidence.

For most people with PD, genes and environment may both contribute—genes load the gun, and environmental exposure pulls the trigger.

Despite remarkable improvements in brain imaging, PD is usually not diagnosed until overt symptoms are present.

At this stage, most of the dopamine nerve cells in the brain areas affected by the disease are already lost, challenging therapies that aim to slow disease progression.

Researchers now know that PD also affects non-dopamine cells in the brain, contributing to the non-movement symptoms.

These symptoms may begin even before the movement problems or emerge in advanced PD.

Non-motor symptoms are receiving increasing attention because they impair quality of life and are not adequately treated by existing therapies.

TOMORROW

Better understanding of genetic and environmental contributions to PD and their interaction will enable physicians and patients to assess personal risk for PD and perhaps take steps to reduce risk.

Intensive efforts are underway to develop biomarkers, which are measurable indicators of the disease process.

Biomarkers will detect PD early, before irreversible damage to the brain, and will speed clinical trials of therapies, reducing the time to test whether new treatments are slowing degeneration from years to months.

In the future, drugs will not just mask PD symptoms, but will slow or stop the underlying degeneration.

Clinical trials supported by NIH and industry are now testing such drugs, including antioxidants, natural nerve cell survival factors, and neurotransmitter-related agents.

Several more drugs designed to interrupt specific molecular steps in the disease process are moving toward clinical testing.

The NET-PD program http://parkinsontrial.ninds.nih.gov/ has already facilitated the review of more than 100 drugs, and the NIH will be supporting a large Phase III clinical trial of creatine, the most promising drug examined to date.

Other NIH-supported trials involve the testing of the antioxidant coenzyme Q10, the fat molecule GM1 ganglioside, and the use of DBS in different brain regions – in order to identify the optimal brain target for stimulation and to provide surgeons with a body of reliable clinical data on which to base their recommendations to patients.

With better knowledge of the role of pesticides and other environmental agents in causing PD, effective prevention will be possible by eliminating or reducing use of specific environmental agents or by developing safe handling equipment and methods that will eliminate exposures that cause PD.

Gene therapy for PD has shown promise in animals and is now moving into first stages of clinical trials in people.

Strategies closest to the clinic, including boosting the capacity of nerve cells to produce neurotransmitters or providing molecules that promote nerve cell survival, may benefit people with inherited or non-inherited PD.

Stem cells may ultimately replace brain cells lost to PD or act as delivery vehicles for nerve cell survival promoting factors, but first uses will be to study the disease process, identify drug targets, and screen potential drugs.

Among ongoing efforts, scientists are exploring induced pluripotent stem cells (iPSCs), which are derived from PD patients’ own skin cells.

Researchers are continuing to advance brain stimulation therapies through improved technology and studies of how DBS affects the brain.

—For example, optogenetics inserts light-sensitive proteins into nerve cells, which allows precise stimulation of brain cells with light pulses.

Scientists are now using optogenetics in animals to understand PD and DBS.

In the future, optogenetics, nanotechnology, and other new technologies may treat PD in people.

Clinicians will also have better treatment options for non-motor features of PD.

Similarly, clinicians, researchers, and people with PD will better understand the broad effects of PD and the overlaps between mechanisms of PD and other diseases, which are becoming increasingly apparent as research determines the molecular steps in neurodegenerative diseases.

Contact: NINDS Brain Resource and Information Network, PO Box 5801 Bethesda, MD 20824, (800) 352-9424

National Institute of Neurological Disorders and Stroke (NINDS) website: http://www.ninds.nih.gov/

http://report.nih.gov/NIHfactsheets/ViewFactSheet.aspx? csid=109

Page Last Updated on February 14, 2011

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