16-08-2011 08:53 Researchers have discovered a new gene mutation they say causes Parkinson's disease. The mutation was identified in a large Swiss family with Parkinson's disease, using advanced DNA sequencing technology. The study, published in the American Journal of Human Genetics, was led by neuroscientists at the Mayo Clinic campus in Florida and included collaborators from the US, Canada, Europe, United Kingdom, Asia and the Middle East. "This finding provides an exciting new direction for Parkinson's disease research," says co-author Zbigniew Wszolek, MD, a Mayo Clinic neuroscientist. "Every new gene we discover for Parkinson's disease opens up new ways to understand this complex disease, as well as potential ways of clinically managing it." The team found that mutations in VPS35, a protein responsible for recycling other proteins within cells, caused Parkinson's disease in the Swiss family. Mutated VPS35 may impair the ability of a cell to recycle proteins as needed, which could lead to the kind of errant buildup of protein seen in some Parkinson's disease brains and in other diseases like Alzheimer's disease says co-author Owen Ross, Ph.D., a neuroscientist at Mayo Clinic in Florida. "In fact, expression of this gene has been shown to be reduced in Alzheimer's disease, and faulty recycling of proteins within cells has been linked to other neurodegenerative diseases," he says. In this video, Dr. Wszolek and Dr. Ross discuss Parkinson's disease and the study.

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Mayo researchers: Genetic mutation linked to Parkinson's disease - Video

09-11-2011 20:24 Andrew Feigin, MD, neurologist at Cushing Neuroscience Institute's Movement Disorders Center and Director of the Experimental Therapeutic at the Feinstein Institute for Medical Research explains the distinctions and brings us the latest information on current treatments and experimental therapies for Parkinson's disease and Huntington's disease. We meet a patient and his caregiver wife who both must cope with living with the under-publicized Huntington's disease everyday.

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Medical Update: Update on Parkinson's

09-11-2011 14:00 Olga Momcilovic speaks at the 2011 CIRM Grantee Meeting about the use of induced pluripotent stem (iPS) cells to better understand the causes of Parkinson's and to develop therapies. Momcilovic is a CIRM Scholar and postdoctoral research fellow at the Buck Institute located in Novato, California.

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Parkinson's Disease: Advancing Stem Cell Therapies - 2011 CIRM Grantee Meeting - Video

Early symptoms of Parkinson's disease include a tremor in the hands, stiff movements and faces that appear to be expressionless. Find out how Parkinson's disease can change a person's speech, balance and gait with help from a nurse and respiratory care practitioner in this free video on Parkinson's disease symptoms.

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Medical Conditions

About the Video: People with neurological diseases, such as Parkinsons disease and Huntingtons disease, may also experience cognitive and emotional symptoms, including anxiety, depression and memory deficits.

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Huntington's and Parkinson's Disease Issues (Part 1)

11-11-2011 17:04

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Marijuana (Hemp) Oil Fights Parkinson's Disease? - Video

Parkinson's Disease Video - Tremor http://www.lloydtan-trust.com

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Parkinson's Disease Video - Tremor

Physical Therapists at Polestar Physical Therapy and Pilates Center in Miami FL use Pilates to help Parkinson's disease patients improve movement and quality of life.

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Polestar Pilates for Parkinson's Disease Patients

Newswise Because there is currently no laboratory test that can diagnose Parkinsons disease, it is practically impossible to detect those individuals who are in the earliest stages of the disease. As a result, Parkinsons disease can only be diagnosed by a clinical neurological examination based on findings suggestive of the disease.

But researchers from the Technion-Israel Institute of Technology Faculty of Medicine have now identified a biomarker comprised of five genes shown to predict Parkinson's disease with high accuracy. The findings are reported in a research article now published online by the scientific journal Molecular Neurodegeneration.

A predictive biomarker for Parkinson's disease could also help to identify high-risk individuals before symptoms develop a stage where prevention treatment efforts might be expected to have their greatest impact to slow disease progression, says lead researcher Dr. Silvia Mandel. It could allow diagnosis of carriers of the genetic risk factors, or those who may exhibit pre-symptomatic stages of the disease [depression, sleep disturbances or hyposmia (reduced ability to smell)] and are good candidates for neuroprotective treatment.

All five genes that comprise the biomarker play a role in the ubiquitin-proteasome system of protein degradation, whose involvement in the pathology of Parkinson's disease has previously been demonstrated.

The study was conducted on blood samples from 62 early stage Parkinson's disease patients and 64 healthy age-matched control subjects. The selection of the genes and determination of their expression in the blood was based on previous research conducted by Dr. Mandel and Prof. Moussa Youdim on the brains of deceased Parkinson's disease patients.

More strikingly, in 30 patients at advanced stages of Parkinson's disease, the model was 100 percent accurate. It was also able to fully discriminate between Parkinson's disease and Alzheimer's disease.

The researchers believe the blood test could one day be combined with brain imaging and/or biomarkers in the spinal fluid or other peripheral tissues, as a gold standard not only for early diagnosis, but also for the differential diagnosis of Parkinson's disease and motor disorders that often mimick the disease symptoms.

Dr. Mandel, who is Vice Director of the Eve Topf Center of Excellence for Neurodegenerative Diseases Research and Teaching at the Technion, conducted the research together with her PhD student Leonid Molochnikov, Professor Youdim; Prof. Judith Aharon of Rambam Medical Center; and Prof. Martin Rabey of Assaf HaRofeh Medical Center. Scientists from the Universities of Wrzburg and Pisa also contributed to the research.

The Technion-Israel Institute of Technology is consistently ranked among the world's leading science and technology universities. Home to three of Israel's five winners of the Nobel Prize in science, the Technion commands a worldwide reputation for its pioneering work in computer science, nanotechnology, biotechnology, energy, water-resource management, medicine, drug development, and aerospace. Headquartered in New York City, the American Technion Society (ATS) promotes scientific and technological research and education at the Technion.

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Researchers ID Cluster of Genes in Blood that Predict Parkinson's

EMERYVILLE, Calif., June 4, 2012 /PRNewswire/ --Adamas Pharmaceuticals, Inc., a privately held company, announced today that it will present an update on its Nurelin (amantadine HCl extended release capsules) program at the Cambridge Healthtech Institute's (CHI) Targeting Parkinson's Disease Symposium being held today in Philadelphia. Nurelin, a once-daily extended release formulation of amantadine intended for night-time administration, is being developed for the treatment of levodopa-induced dyskinesia (LID) in Parkinson's disease (PD) patients. Results from the Company's prior Phase 1 studies, its preclinical program in Parkinson's and other indications, along with a status report on the ongoing Phase 3 study, Extended Release Amantadine Safety and Efficacy Study in Levodopa-Induced Dyskinesia (EASED), will be presented by Gregory T. Went, Ph.D., Co-Founder and Chief Executive Officer of Adamas. The talk is entitled, "Exploring the Potential of Modified Release Aminoadamantanes in Parkinson's Disease and Related Indications."

"We are excited to introduce the Nurelin program at the conference today, and to provide an update on the previous preclinical and clinical studies that have led to our first Phase 2/3 study of Nurelin in Parkinson's patients who experience levodopa-induced dyskinesia," said Dr. Went. "Amantadine is a remarkable drug that has received little attention from the pharmaceutical industry for the past 30 years, and we hope the EASED study of Nurelin, combined with recently presented academic studies in Parkinson's disease, will help establish new treatment indications for Nurelin. We look forward to presenting the results from this study and assessing the potential of Nurelin as our second NDA candidate to Arimenda."

There are no medications currently approved for the treatment of levodopa-induced dyskinesia, thus there is a significant unmet medical need. Pending the outcome of the EASED study and regulatory review, Nurelin may become the first drug indicated for the treatment of levodopa-induced dyskinesia in Parkinson's disease. Nurelin also is being investigated as a therapeutic agent to address the non-motor symptoms of Parkinson's disease, including fatigue.

About Nurelin (ADS-5102)

Nurelin (ADS-5102) is a proprietary formulation of amantadine in development for the treatment of central nervous system (CNS) disorders including LID in PD patients. Nurelin is designed for once daily administration at night and is being investigated at plasma concentrations up to 2.5 fold higher than those achievable with the commercially available immediate release amantadine tablets. Nurelin capsules can be opened and the contents sprinkled on food for ease of administration in patients who have difficulty swallowing capsules.

Nurelin has a pharmacokinetic profile designed to overcome the CNS side effects associated with immediate release forms of amantadine, while offering potential for enhanced efficacy. This novel pharmacokinetic profile of Nurelin is characterized by: i) higher plasma concentrations during the daytime hours when the motor and non-motor symptoms of Parkinson's disease are at their peak; ii) low plasma concentrations overnight, which may reduce sleep disturbance and vivid dreams occasionally associated with amantadine; and iii) a reduced initial rate of rise in plasma concentration, which is expected to improve overall CNS tolerability of amantadine.

The efficacy and tolerability of multiple doses of Nurelin in the treatment of LID in Parkinson's disease patients is currently being studied in a Phase 2/3 study. This study, entitled EASED (Extended Release Amantadine Safety and Efficacy Study in Levodopa-Induced Dyskinesia), is designed to evaluate the efficacy of three dose strengths of Nurelin for the treatment of LID, and to confirm the tolerability of the new formulation (www.easedPD.com).

About LID in Parkinson Disease

Parkinson's disease is a chronic, progressive disorder with prominent motor signs including tremors, rigidity, bradykinesia and postural instability. Levodopa, the most commonly prescribed and effective drug treatment for symptomatic relief in PD is associated with dose limiting motor side effects, including abnormal involuntary, dance-like movements known as dyskinesia. With continued levodopa treatment, and as PD progresses, dyskinesia can become severely disabling and has been associated with a decrease in the quality of life.

About Adamas

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Adamas Pharmaceuticals Presents Update On Nurelin™ Program At Cambridge Healthtech Institute's Parkinson's Conference

A devastated Michael J. Fox initially turned to alcohol to cope with his Parkinson's disease diagnosis.

The Family Ties star discovered he had the degenerative disorder back in 1991 and confesses he took to the bottle to drown his sorrows.

He tells Parade magazine, "For a time I dealt with it with alcohol, which turned out to be a disaster. I'd always been kind of a partier, but this was the first time I was drinking in order not to feel something. It had a dark purpose."

The actor eventually quit drinking for good and now Fox credits his wife of 23-years, Tracy Pollan, with helping him get sober.

He continues, "About a year after my diagnosis, I woke up one morning and saw (wife) Tracy's face...She said, 'Is this what you want?' Instantly I knew - no, this isn't what I want or who I am. So I quit drinking in '92.

"I recognised I had choices about drinking, and that made me realise I had choices about Parkinson's as well... Acceptance doesn't mean resignation; it means understanding that something is what it is and that there's got to be a way through it."

Fox has been a longtime Parkinson's disease advocate and in 2000 he founded The Michael J. Fox Foundation, which funds research programmes in the hopes of finding a cure.

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Fox turned to alcohol to cope with Parkinson's disease

KINGSTON, N.J., May 2, 2012 /PRNewswire/ --The 18th Annual Parkinson's Unity Walk (PUW), held on Saturday, April 28, 2012 in New York City's Central Park, raised more than $1.5 million thus far and united 10,000 walkers, The Parkinson Alliance announced today.

The event, kicked-off by Michael J. Fox, drew a record number of 527 registered teams participating in the PUW's 18 year history to help raise funds for Parkinson's disease (PD) research. The funds raised are distributed evenly among the nation's seven leading Parkinson's foundations, and the PUW will continue to accept contributions for the 2012 event through May 28, 2012.

A number of leading advocates and representatives from the Parkinson's community spoke at the PUW, including Congresswoman Carolyn Maloney, 14th CD; Michael Jones, Divisional VP & General Manager, Abbott; May May Ali, Writer and Comedian; and Martin Tuchman, Chairman of the Parkinson's Unity Walk.

"Collaboration and sharing two words that are extremely important to the success of this community," said Carol Walton, Chief Executive Officer of The Parkinson Alliance. "People living with Parkinson's, researchers, healthcare professionals, volunteers and foundations all working together to assure that one day a year, the most comprehensive day of community and education takes place for people with Parkinson's and their families."

The PUW is the largest awareness and fundraising event for PD research in the United States.

"The Parkinson's Unity Walk is important, not only for members of the Parkinson's community but also for the field of Parkinson's disease research," said Todd Sherer, Chief Executive Officer of the Michael J. Fox Foundation for Parkinson's Research. "It brings together so many of us who are deeply invested in finding a cure, and the funds raised help speed progress for patients today. The Michael J. Fox Foundation is grateful to be a part of this inspiring event."

For Walk participants, the PUW represented much more than a one-day event. It was an opportunity for patients, caregivers and organizations to all come together in support of the community.

"Year after year, I'm humbled by the consistent support from my friends, family and colleagues," said Jim McNasby, Team Captain of top fundraising team, Team McMoss, and PUW Board Member. "Their generosity is both extraordinary and impactful because all of the donations go directly to research. And when I hear about the research especially some of the genetic research supported by the Walk it gives me hope for the future. Hope keeps me going."

In addition to individual and team fundraising efforts, Abbott, a leading global health care company and premier sponsor of the PUW, helped raise an additional $30,000, which will be donated directly to the PUW in support of research.

Additional sponsors included Boehringer Ingelheim, Teva CNS, Chelsea Therapeutics, LSVT Global, Medtronic, Novartis, and UCB.

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18th Annual Parkinson's Unity Walk Raises More Than $1.5 Million in Support of Parkinson's Research

Editor's Choice Main Category: Parkinson's Disease Article Date: 02 May 2012 - 11:00 PDT

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By using powerful computer tools and laboratory tests, the scientists managed to obtain a step-by-step explanation of how a "protein-run-amok" aggregates within the membranes of neurons, puncturing them and causing Parkinson's disease symptoms. The process describes how -synuclein (a-syn) can turn against us, especially as we get older. The results of the model demonstrate how -syn monomers penetrate cell membranes and how they become coiled and aggregate within nanoseconds into dangerous ring structures that are harmful for neurons.

Lead researcher Igor Tsigelny, a research scientist at the San Diego Supercomputer Center and Department of Neurosciences at UC San Diego, declared:

Numerous cases of familial Parkinson's disease are caused by a limited number of protein mutations, the most toxic of which is A53T. Tsigelny's team demonstrated that the mutant form of -syn both penetrates neuronal membranes substantially faster compared with a normal -syn, and that the mutant protein also accelerates ring formation.

Tsigelny explained:

The researchers discovered that their modeling results also proved consistent with electron microscopic images of neurons in Parkinson's disease patients that have shown damaged neurons are riddled with ring structures.

The researchers immediately turned to search for drug candidates that can inhibit ring formation in neuron membranes. The highly complex modeling consists of various sophisticated scientific realms, which intersect between chemistry, physics, and statistical probabilities. A wide spectrum of interacting forces within this realm cause circumstances comparable to an earthquake, in which the a-syn proteins bump and tremble, coil and uncoil and join up in pairs or larger groups.

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Once-Marginalized Parkinson's Disease Theory May Be Valid

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April is Parkinson's Awareness Month-Parkinson Society Canada Encourages Canadians With Parkinson's to Get Active, Get ...

Despite researchers' best efforts, Parkinson's disease remains incurable. While there are treatment options that mitigate some symptoms, assigning the right treatment approach can be hit or miss. To better predict the response of Parkinson's patients to therapy, the Cleveland Clinic has joined consumer genomics company 23andMe in its Parkinson's Community Research Project. Enrollment in the program will also allow the clinic's patients to take advantage of 23andMe's Personal Genome Service.

23andMe began its Parkinson's disease collaboration in 2009 when it teamed up with the Michael J. Fox Foundation for Parkinson's Research and the Parkinson's Institute and Clinical Center. After roughly 18 months, the collaboration had assembled and analyzed genetic data from more than 3,400 Parkinson's patients, found 20 previously known genetic associations, and identified two novel loci rs6812193 near SCARB2 and rs11868035 near SREBF1/RA11. Ultimately, the collaboration aims to enroll 10,000 people. To date, 23andMe has enrolled roughly 6,500 patients, and the Cleveland Clinic is planning to add another 1,000 patients.

For clinicians like Andre Machado, director of the Cleveland Clinic's Center for Neurological Restoration, the ideal scenario is that this large-scale collaboration can produce a roadmap to advance treatments for Parkinson's patients. "We're hoping to get data on the progression or responsiveness to a given type of treatment, things that can help us understand maybe in the future how to select treatments that are more likely to work for some patients versus others," Machado says.

The process starts by reaching out to patients diagnosed with Parkinson's disease by their neurologists and inviting them to participate. "Because this study aims to find novel genetic variants associated with Parkinson's disease by way of genome-wide association studies, it is crucial that the group of whose genes are being analyzed have a pure diagnosis of Parkinson's disease, as opposed to parkinsonism," says Kathryn Teng, director of the Center for Personalized Healthcare at the Cleveland Clinic. "As with all genome-wide association studies, in order to get pure results, you need to have pure data going into the study."

One enrollment challenge, Teng says, is that participants might be older, and therefore less comfortable with computers. "The 23andMe model requires electronic enrollment and participation in surveys, so family members may need to assist with the enrollment and data collection if the patient requires assistance," she adds.

Reaching the desired sample size is also made difficult by a lack of -familiarity with genetic research in some pockets of the target population. "Many may not be aware of the protections offered by the GINA law which protects against discrimination based on genetic information for health insurance and employment," Teng says. To assuage any anxieties, potential recruits are told that they and their DNA samples will only be identified by a unique code. They are also told that the reports that they receive through 23andMe's website summarizing the genes identified in their DNA will not be part of their medical record.

To make participation as easy as possible, the Cleveland Clinic has dedicated computer portals set up at locations where Parkinson's patients are likely to visit, including its various campuses.

Ultimately, Machado says he does not know if 10,000 patients will be a large enough sample size to effectively interrogate the data to make a difference on treatment. However, he adds, the collaboration with 23andMe provides "an opportunity for doing exploration and there is a chance that it will benefit patients down the line."

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Recruits for Research

Posted: Sunday, April 1, 2012 4:00 am | Updated: 4:55 pm, Wed Mar 28, 2012.

OPTIMISM is the focus of this years annual American Parkinson Disease Association East Texas OPTIMISM Walk 2012, scheduled April 28 at the Rose Rudman Recreational Trail in Tyler.

The East Texas Parkinsons walk is an annual effort to raise money for education, research and support services for those affected by Parkinsons disease. The event is sponsored by the APDA East Texas Chapter and the ETMC Movement Disorder Center.

Individuals living with Parkinsons or those whose friends or loved ones have been diagnosed and all individuals who want to support a good cause are invited to join in by registering for or donating to our event today, said Kelly Boutin, walk chairperson and Tyler-area APDA Information and Referral Center coordinator. When everyone works together, great things can be accomplished to ease the burden and find the cure for Parkinsons disease.

The Tyler walk is open to all East Texas residents, and it starts at 11:30 a.m. on April 28 in the Robert E. Lee parking lot near the REL track. Check-in starts at 10 a.m. All activities will conclude at 2 p.m.

Approximately 3.6 million Americans have been diagnosed with Parkinsons disease. Approximately 50,000 new cases are diagnosed each year, and many more may have Parkinsons without realizing it yet.

It predominantly affects older adults, but healthcare providers also see early onset cases, which are estimated at between five and 10 percent of the total Parkinsons population.

For more information, or to support or participate in the Optimism Walk for Parkinsons, visit our chapter website at http://www.etapda.org or contact: Kelly Boutin at 903-596-3618 or kmboutin@etmc.org.

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East Texas Optimism Walk for Parkinson’s disease set for April 28

LONGMONT -- Shake tambourines. Dance like a gypsy.

Now do it when you are struggling with Parkinson's disease, a progressive neurological disorder that can cause tremors, sluggishness and rigidity.

That's what Stephen Straub asks of his students every Wednesday afternoon during the "Movin' with Parkinson's" class at the Longmont Dance Theatre.

Where: Longmont Dance Theatre, 1422 Nelson Road, Longmont

When: 1 to 2 p.m. Wednesdays

Cost: $5

To register: Call 303-830-1839 or email Info@ParkinsonRockies.org.

More information: Visit ParkinsonRockies.org

Two years ago, Straub traveled to Brooklyn, N.Y., to take a two-day training program called Dance for PD at the Mark Morris Dance Group. The National Parkinson Foundation commissioned renown ballet choreographer Morris to use dance to engage Parkinson's patients.

Only 40 communities worldwide offer the class made available in Longmont last fall, said Kari Buchanan, spokeswoman for Denver-based Parkinson Association of the Rockies.

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Longmont a select city for creative Parkinson's disease dance class

For years, doctors have treated the Parkinson's disease symptoms they could see: the shaking hands, the stumbling feet.

But one of the likely causes of Parkinson's is almost invisible. It's buried deep within brain cells, where tiny engines called mitochondria slowly are shutting down.

Now a team of researchers at Virginia Commonwealth University, and a biotech company in Charlottesville, say they think they've found a way to rev up those engines once again, potentially reversing the disease.

Every cell in your brain is packed with mitochondria tiny engines that generate the energy cells need to function. But sometimes these brain cells do a curious thing. They turn off the signals to make mitochondria, depriving themselves of power. The tiny engines sputter and eventually cease to operate.

Essentially, "the brain is divorcing its mitochondria," says Dr. James P. Bennett Jr., director of the university's Parkinson's Disease and Movement Disorders Center. This, scientists recently discovered, appears to be a likely root cause of Parkinson's disease, Alzheimer's disease, and other heretofore mysterious brain disorders.

In 2004 one of Bennett's graduate students, Shaharyar Khan, developed a way to deliver healthy mitochondrial DNA directly into mitochondria via a protein carrier. In mice and cultured human cells, this method of gene therapy has been shown to revive the mitochondria, restoring the cell to normal function.

"It's novel," Bennett says. "No one else has it."

In January the researchers asked the U.S. Food and Drug Administration for approval to begin human clinical trials. The approval process may take a while, but Bennett's optimistic the team will be able to begin the trials this year.

One of Bennett's colleagues, Dr. Patricia A. Trimmer, is pursuing another promising therapy for Parkinson's patients: near-infrared laser light. The laser beam painlessly penetrates a person's skull, stimulating brain cells and rousing their sluggish mitochondria.

Trimmer shows speeded-up video clips of two sets of mitochondria, which look like tiny white rods traversing a long, narrow nerve cell. In the first video, they creep like rush-hour traffic. In the second video, after being treated with the laser light, they're zipping around like go-karts.

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The Brain-Makers

12-10-2011 04:21 Demonstration of early stage secondary Parkinson's disease symptoms (slurry speech, trouble initiating movements, loosing balance) on a 30 year old woman, who lost almost all of her putamen (part of the basal ganglia) on both sides of the brain resulting from the lack of oxygen in the injured part of her brain. The professional term for her injury is anoxic-ischemic brain injury. You can read up her story and make donations here: http://www.gofundme.com Join the free Facebook group I set up for her for following updates (www.facebook.com Date of Accident: June 7th, 2011. Video taken: Oct. 12th, 2011

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Emese's (30) early stage secondary Parkinson's disease symtoms (anoxic-ischemic brain injury) - Video

23-09-2011 12:02 Mark Morris Dance Group performed in Ann Arbor Sept 23-24, 2011 as part of UMS's 11/12 Season. In this interview, David Leventhal discusses Dance for PD, an on-going collaboration between the Mark Morris Dance Group and the Brooklyn Parkinson Group.

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Mark Morris Dance Group: Dance for Parkinson's Disease - Video