MERIDIAN When the Meridian Parkinson's Disease Support Group first met a few months ago there were only four people in attendance who suffer from the debilitating condition.

The last meeting of the group saw 50 people show up looking for mutual support, information and peace of mind. Needless to say, Jimmy Gossett, one of the founding members of the group, was both astonished and pleased at the response.

"It is so nice to meet so many people who have the same condition as you," said Gossett, explaining he doesn't wish the disease on anyone. "But when you have this kind of problem, having friends and meeting new ones who through sheer numbers can build you back up, that is a nice thing."

With each new group meeting, Gossett said more and more health professionals work to assist in any way they can. Gossett said in the upcoming meeting, set forTuesday, June 12 at 10 a.m.at the Fifteenth Avenue Baptist Church in Meridian, three health professionals will be on hand to lend their expertise in the realm of Parkinson's Disease (PD).

"We will have physical therapists and speech pathologists on hand to help with information on what we face as PD sufferers," Gossett said. "But we will have fun, laugh, and fellowship. That is the best therapy we can have."

Gossett said the therapists will bring with them years of experience in dealing with PD sufferers. He said the health professionals will address such issues as speech deficits including reduced volume in their voices, decreased intelligibility, poor breath support and swallowing. Speech pathologists Angela Ramsey and Lesley Smith will be speaking to the group about oral motor exercises, respiratory exercises, and patterning techniques. The subject of neuromuscular e-stim to improve speech and swallowing will be covered.

Also, Amanda Sayers, a physical therapist, will be on hand to discuss some exercise techniques and different treatment approaches for the group as related to gait patterns, how to deal with "freezing" and tremors, and safety precautions.

"Each of these presentations will be followed by question and answer sessions so each person there can get the answers unique to their conditions," said Gossett.

Gossett said everyone is invited. He said he hopes that all PD suffers, not only in Meridian and Lauderdale County, but also throughout the East Mississippi area, will come and discover this group so they can seek the help and support so many sufferers need.

"It is all up to us, the PD sufferer, to increase our knowledge and understanding of this condition so that we can better cope with it," Gossett said. "We encourage those family members who have a person suffering from PD to come as well so they can get a firm grip on what their loved one is going through."

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Parkinson's group to meet

State Rep. John Robinson (D-Scottsboro) said on Thursday he is in the early stages of Parkinson's Disease.

Robinson said he was diagnosed in January, shortly before the start of the 2012 Alabama Legislative Session.

"I'm on medication," said Robinson. "It's not a death sentence. It's treatable, but not curable."

Currently serving his fifth term in office after first being elected in 1994, Robinson said he only missed two days of the legislative session this year.

Parkinson's Disease is a chronic, degenerative neurological disorder that affects one in 100 people over age 60. It leads to shaking (tremors) and difficulty with walking, movement and coordination.

Robinson said he's had no problems with shaking.

"It gets my voice," he said. "And my coordination when I'm walking."

Robinson said he is going this summer to see a special neurologist in Chicago, one who has treated Muhammed Ali and Michael J. Fox.

Robinson, who retired from the Jackson County District Attorney's Office after entering politics, will complete 20 years in office when his current term ends. His five terms as state representative is the most for a person from Jackson County.

"I'm proud of that," he said.

Originally posted here:
Robinson diagnosed with Parkinson's Disease

Public release date: 4-Jun-2012 [ | E-mail | Share ]

Contact: Kagan Kerman kkerman@utsc.utoronto.ca 416-287-7249 University of Toronto Scarborough

Researchers at the University of Toronto Scarborough (UTSC) used an innovative technique to examine chemical interactions that are implicated in Parkinson's Disease.

The work details how a protein called alpha-synuclein interacting with the brain chemical dopamine can lead to protein misfolding and neuronal death.

Parkinson's Disease is a neurodegenerative disease which results in loss of motor control and cognitive function. Although the cause isn't known precisely, the disease involves the death of brain cells that produce dopamine, a chemical important in neuronal signaling. The disease also involves a protein called alpha-synuclein which aggregates in the neurons of people with the disease.

Kagan Kerman, a chemist in the Department of Physical and Environmental Sciences, and Ian R. Brown, a neuroscientist who founded UTSC's Centre for the Neurobiology of Stress in the Department of Biological Sciences, looked at the way dopamine interacts with alpha-synuclein to form aggregates that may be toxic to neurons.

"This is very fundamental," says Kagan Kerman. "It gives us a new point of view of the misfolding proteins and how they are affected by dopamine."

These sorts of interactions are often studied using microscopy. But the UTSC researchers decided to use an electroanalytic technique called voltammetry. By studying tiny changes in electric current as dopamine and alpha-synuclein interacted they were able to determine details about the early phases of the interaction.

Using the technique, they were able to detail how changes in pH levels and ionic strength of the solution affected the interaction. They found that at higher pH levels and higher ionic strengths, dopamine interacted much more strongly with alpha-synuclein, forming aggregates more quickly.

The results could have implications for understanding and treating the disease. Normally dopamine is contained in structures called vesicles, in which pH levels are low and dopamine is unlikely to interact with alpha-synuclein. Outside of the vesicles dopamine encounters higher pH levels and, according to the new research, is much more likely to interact to create aggregates.

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New research yields insights into Parkinson's disease

Public release date: 23-May-2012 [ | E-mail | Share ]

Contact: Mike Morrison mdmorrison@partners.org 617-724-6425 Massachusetts General Hospital

Use of the antioxidant urate to protect against the neurodegeneration caused by Parkinson's disease appears to rely on more than urate's ability to protect against oxidative damage. In the May issue of the open-access journal PLoS One, researchers from the MassGeneral Institute for Neurodegenerative Diseases (MGH-MIND) describe experiments suggesting the involvement of a novel mechanism in urate's protection of cultured brain cells against Parkinson's-like damage.

"Our experiments showed, unexpectedly, that urate's ability to protect neurons requires the presence of neighboring cells called astrocytes," says Michael Schwarzschild, MD, PhD, of MGH-MIND, the study's senior author. "The results suggest there may be multiple ways that raising urate could help protect against neurodegeneration in diseases like Parkinson's and further support the development of treatments designed to elevate urate in the brain." Schwarzschild and colleagues in the Parkinson's Study Group currently are conducting a clinical trial investigating one approach to that strategy.

Characterized by tremors, rigidity, difficulty walking and other symptoms, Parkinson's disease is caused by destruction of brain cells that produce the neurotransmitter dopamine. Several epidemiological studies suggested that healthy people with elevated levels of urate, a normal component of the blood, may have a reduced risk of developing Parkinson's disease, and investigations by Schwarzschild's team found that Parkinson's patients with higher naturally occuring urate levels had slower progression of their symptoms.

The current study was designed to investigate whether both added urate and urate already present within the cells protect cultured dopamine-producing neurons against Parkinson-like degeneration. In addition, since previous studies suggested that urate's protective effects depended on the presence of astrocytes star-shaped cells of the central nervous system that provide both structural and metabolic support to neurons the MGH-MIND team explored how the presence of astrocytes affects the ability of urate to protect against damage induced by MPP+, a toxic molecule that produces the same kind of neurodegeneration seen in Parkinson's and is widely used in research studies.

The experiments showed that, while added urate reduced MPP+-induced cell death by about 50 percent in cultured dopamine-producing mouse neurons, urate treatment virtually eliminated neuronal death in cultures containing both neurons and astrocytes. They also showed that reducing intracellular urate levels by induced expression of the enzyme that breaks it down increased neuronal vulnerability to MPP+ toxicity significantly in cultures that included astrocytes but only slightly in neuron-rich cultures. The fact that the presence of astrocytes greatly increases the protection of both externally applied urate and urate produced within cells indicates that the effect depends on more than urate's ability to directly protect neurons against oxidative stress.

"A valuable next step will be determining whether endogenous urate is protective in live animal models of Parkinson's disease," says Schwarzschild. "It also will be important to determine whether we can selectively increase urate levels in brain cells by targeting urate transporter molecules. The approach now in early clinical trials examines whether treatment with the urate precursor inosine, which increases urate levels throughout the body, can slow the progression of the disease. If we could raise urate levels in brain cells without changing them in the rest of the body, we could avoid the risks of of excessive urate, which when accumulated in joints can cause gout."

###

Schwarzschild is an associate professor of Neurology at Harvard Medical School. Sara Cipriani, MD, of MGH-MIND is the lead and corresponding author of the PLoS One report. The study was supported by grants from the National Institutes of Health, the Department of Defense and the American Parkinson's Disease Association.

Read this article:
Study supports urate protection against Parkinson's disease, hints at novel mechanism

This multicentre, parallel, double-blind, placebo-controlled, randomised trial was done in 13 movement disorders departments in France between October, 2009, and December, 2011. Eligible patients were younger than 80 years and had Parkinson's disease, severe gait disorders, and freezing of gate despite optimised treatment of motor fluctuations with dopaminergic drugs and subthalamic stimulation. We randomly assigned patients (1:1 with a computer random-number generator in blocks of four) to receive methylphenidate (1 mg/kg per day) or placebo capsules for 90 days. Patients, their carers, study staff, investigators, and data analysts were masked to treatment allocation. To control for confounding effects of levodopa we assessed patients under standardised conditions with an acute levodopa challenge. Our primary outcome was a change in the number of steps during the stand-walk-sit (SWS) test without levodopa. We compared the respective mean numbers of steps at day 90 in the methylphenidate and placebo groups in a covariance analysis and adjusted for baseline differences. This trial is registered with ClinicalTrials.gov, number NCT00914095.

Read more from the original source:
Methylphenidate for gait hypokinesia and freezing in patients with Parkinson's disease undergoing subthalamic ...

KUSA - If you or someone you know has Parkinson's disease (PD) you are not alone. In the United States, as many as 60,000 cases of PD are diagnosed each year. Our morning show devoted a full call-in to the topic on Thursday.

We had Parkinson's disease specialists in our information center, along with the President of the Parkinson Association of the Rockies.

The experts say (PD) is a neurodegenerative brain disorder that progresses slowly in most people. What this means is that individuals with PD will be living with PD for twenty years or more from the time of diagnosis.

While Parkinson's disease itself is not fatal, the Center for Disease Control rated complications from the disease as the 14th top cause of death in the United States. There is currently no cure for Parkinson's; however, there are treatments that help control the symptoms of PD and can give those afflicted with it, a good quality of life.

Learn more by visiting:http://www.parkinsonrockies.org/

(Copyright 2012 by The Associated Press. All Rights Reserved.)

Original post:
Latest Doctor Line9: Parkinson's

WAPELLO, Iowa Riding a motorcycle takes a steady hand. Although Jeff Weikert doesnt have that luxury anymore, that wont stop him from riding.

In 2009, Weikert, 51, of Wapello, was diagnosed with Parkinsons disease, a degenerative disorder of the central nervous system. The disease hasnt stopped him from riding, though.

The career motorcycle and stock car racer signed up to participate in the 90th edition of the Pikes Peak International Hill Climb, also known as the Race to the Clouds, in Colorado Springs, Colo.

To participate, one has to submit a resume of personal racing history. After Weikert submitted his on Dec. 1, 2011, his wife, Angie, 46, said they were invited to participate in the race.

Its fine with me, and hes been racing since Ive known him, Angie said. Its one more race that was on his bucket list.

Angie said the last race that her husband participated in was in 2010 for District 17, an American Motorcycle Association organization that competes in Illinois. She described that race as featuring specialty made cycles through an obstacle course.

Its timed, but slow and about balancing, Angie said. His Parkinsons prevented him from competing again after he was diagnosed.

For the race in Colorado, Weikert will ride a 1974 Honda 250cc motorcycle. The cycle was built and is owned by Paynes Cycle Center in Rock Island. He is only one of two riders from Iowa to compete in the 200-man race.

Heading to Colorado with Jeff and his wife for the race on July 8 are their two sons, Jonathan and Jacob and Jacobs wife, Jessica. Others include members of Paynes Cycle Center and other friends and family to help with their fundraising.

After Jeff was diagnosed, he and his wife sought information about the disease through the Michael J. Fox Foundation for Parkinsons Research. For the race, the Weikerts have teamed up with the foundation to help raise awareness and money.

Original post:
Man's 'Race to the Clouds' will help fight Parkinson’s disease

by Sylvia Perez and Christine Tressel

May 24, 2012 (CHICAGO) -- Colonoscopies are known for detecting early signs of cancer in the colon. Now Chicago researchers say this common test may help reveal who might be at risk of developing Parkinson's disease. They have discovered a clue in the gut that could be a game changer for early diagnosis and even treating the disease.

Richard Fiske Bailey says even he had a hard time realizing something was happening with his body. It was the way he was driving his sports car that caught the attention of friends.

"When I went to shift gears I would reach down with my left hand and shift I would shift with my left hand instead of my right hand, I never noticed it. And people would start to say, what is wrong," Fiske said.

It took a long time but eventually he had a diagnosis: Parkinson's disease.

"I was formally diagnosed in 2003 by my fifth neurologist," Fiske said.

A slight tremor in a hand, tense muscles and slow movements are some of the more distinctive signs suggesting Parkinson's disease. But even these can be confused with other conditions. That means thousands of cases are not diagnosed until a lot of brain cells are gone.

Parkinson's disease occurs when the nerve cells in the brain that make a chemical called dopamine are slowly destroyed. No one is sure why that happens.

Now researchers are turning to what would seem an unlikely source of a brain disorder: the gut.

"This area of research is really hot right now, and we think it's really important," said Dr. Kathleen Shannon, neurologist, Rush University Medical Center

More:
Healthbeat Report: Predicting Parkinson's

Horse lover had become depressed after condition meant she could no longer ride Inquest told she could not accept that the things she liked were becoming more and more difficult Losing driving licence was the 'final straw'

By Phil Vinter

PUBLISHED: 15:23 EST, 7 May 2012 | UPDATED: 15:28 EST, 7 May 2012

A mum committed suicide on the day her driving licence was revoked because Parkinson's Disease symptoms had become too bad.

Karen Bottrill, 51, hung herself following the DVLA (the vehicle licencing agancy) at a spot where her beloved daughter used to play as a child.

An inquest heard that Mrs Bottrill had requested space after leaving her home at Larkhill, in Salisbury Plain, Wiltshire, following the news.

Crushing news: Salisbury Coroner's Court heard that Karen Bottrill hung herself after the DVLA deemed her unable to drive a car because of her debilitating Parkinson's symptoms

Yesterday her husband Gordon, 50, said the DVLAs decision to ban her from driving was the final straw for his wife, after losing the ability to continue her passion for riding horses.

Mr Bottrill said Karen - who was first diagnosed with the debilitating nerve condition in 2006 - could not accept that all of the things she liked were becoming more and more difficult.

See more here:
Distraught Parkinson's sufferer killed herself when driving licence was revoked

Public release date: 11-May-2012 [ | E-mail | Share ]

Contact: Patrik Verstreken 32-497-422-165 VIB (the Flanders Institute for Biotechnology)

Neuroscientist Patrik Verstreken, associated with VIB and KU Leuven, succeeded in undoing the effect of one of the genetic defects that leads to Parkinson's using vitamin K2. His discovery gives hope to Parkinson's patients. This research was done in collaboration with colleagues from Northern Illinois University (US) and will be published this evening on the website of the authorative journal Science.

"It appears from our research that administering vitamin K2 could possibly help patients with Parkinson's. However, more work needs to be done to understand this better," says Patrik Verstreken.

Malfunctioning power plants are at the basis of Parkinson's.

If we looked at cells as small factories, then mitochondria would be the power plants responsible for supplying the energy for their operation. They generate this energy by transporting electrons. In Parkinson's patients, the activity of mitochondria and the transport of electrons have been disrupted, resulting in the mitochondria no longer producing sufficient energy for the cell. This has major consequences as the cells in certain parts of the brain will start dying off, disrupting communication between neurons. The results are the typical symptoms of Parkinson's: lack of movement (akinesia), tremors and muscle stiffness.

The exact cause of this neurodegenerative disease is not known. In recent years, however, scientists have been able to describe several genetic defects (mutations) found in Parkinson's patients, including the so-called PINK1 and Parkin mutations, which both lead to reduced mitochondrial activity. By studying these mutations, scientists hope to unravel the mechanisms underlying the disease process.

Paralyzed fruit flies

Fruit flies (Drosophila) are frequently used in lab experiments because of their short life spans and breeding cycles, among other things. Within two weeks of her emergence, every female is able to produce hundreds of offspring. By genetically modifying fruitflies, scientists can study the function of certain genes and proteins. Patrik Verstreken and his team used fruitflies with a genetic defect in PINK1 or Parkin that is similar to the one associated with Parkinson's. They found that the flies with a PINK1 or Parkin mutation lost their ability to fly.

Upon closer examination, they discovered that the mitochondria in these flies were defective, just as in Parkinson's patients. Because of this they generated less intracellular energy energy the insects needed to fly. When the flies were given vitamin K2, the energy production in their mitochondria was restored and the insects' ability to fly improved. The researchers were also able to determine that the energy production was restored because the vitamin K2 had improved electron transport in the mitochondria. This in turn led to improved energy production.

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Vitamin K2: New hope for Parkinson's patients?

Public release date: 2-May-2012 [ | E-mail | Share ]

Contact: George Hunka ghunka@aftau.org 212-742-9070 American Friends of Tel Aviv University

Parkinson's disease, a disorder which affects movement and cognition, affects over a million Americans, including actor Michael J. Fox, who first brought it to the attention of many TV-watching Americans. It's characterized by a gradual loss of neurons that produce dopamine. Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson's symptoms at a young age.

The ability to modify the activity of DJ-1 could change the progress of the disease, says Dr. Nirit Lev, a researcher at Tel Aviv University's Sackler Faculty of Medicine and a movement disorders specialist at Rabin Medical Center. Working in collaboration with Profs. Dani Offen and Eldad Melamed, Dr. Lev has now developed a peptide which mimics DJ-1's normal function, thereby protecting dopamine- producing neurons. What's more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.

Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. Dr. Lev says that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.

Guarding dopamine levels

As we age, we naturally lose dopamine-producing neurons. Parkinson's patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson's patient or aging normally, says Dr. Lev.

The researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle. "We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain," explains Dr. Lev.

In pre-clinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson's disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.

Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this peptide does not. Additionally, it provides a safe treatment option because peptides are organic to the body itself.

Read more here:
Freezing Parkinson's in its tracks

Public release date: 3-May-2012 [ | E-mail | Share ]

Contact: Dennis Tartaglia dtartaglia@tartagliacommunications.com 732-545-1848 Tartaglia Communications

Samuel M. Young, Jr., PhD, research group leader at the new Max Planck Florida Institute (MPFI), has received his first grant from The Michael J. Fox Foundation for Parkinson's Research (MJFF). The grant will enable Dr. Young and colleagues to develop a technology that will help scientists working in drug development to research potential treatments that target LRRK2, a Parkinson's-related gene. Globally, five million people have Parkinson's disease.

"We are excited about receiving The Michael J. Fox Foundation grant, as these grants are competitive and MJFF is the world's largest private funder of Parkinson's research," said Dr. Young, who directs MPFI's Molecular Mechanisms of Synaptic Function research group. "We believe that the tools we develop will prove important in advancing Parkinson's research."

Translational researchers working in Parkinson's disease have been hindered in studying the function of the LRRK2 gene in pre-clinical models of Parkinson's. This has been due to difficulty in expressing this gene with commonly used neuroscience research tools known as recombinant viral vectors. Dr. Young will develop tools that will allow researchers to get around this problem.

Mutations in the gene for leucine-rich repeat kinase 2 (LRRK2) are among the most common genetic links to Parkinson's disease yet discovered. LRRK2 has garnered much excitement among drug makers due to its reported protein kinase activity, which appears to be enhanced by Parkinson's disease-causing mutations.

"We are delighted that The Michael J. Fox Foundation has awarded Dr. Young with a grant to lead this critical project," said David Fitzpatrick, PhD, CEO and Scientific Director of MPFI. "This grant recognizes Dr. Young's specialized expertise, as well as our Institute's leadership role in neural circuit research."

Recombinant viral vectors are used by scientists to deliver genetic material into cells. Viruses have evolved specialized molecular mechanisms to efficiently transport their genomes inside the cells they infect. To create the vector, viruses are bioengineered to strip their viral genome or most of their viral genome, which renders them harmless. This enables them to carry transgene expression cassettes to express a gene of interest. The transgene expression cassette is a fragment of DNA that carries the regulatory elements necessary for cells to express specific genes within a cell or organism.

As the principal investigator of the project, Dr. Young will work with collaborators at other institutions to generate the optimal expression cassette to express LRRK2.

Dr. Young has specialized training that makes him the ideal investigator for this project. After training in virology and in recombinant viral vectors during his doctoral studies, Dr. Young switched fields and became a post-doctoral neuroscience researcher, learning electrophysiology techniques. He carried out a second post-doctoral position, gaining further experience with advanced electrophysiological techniques as well as calcium imaging. Using this unique training, which combines techniques in molecular, electrophysiological and biophysical methods, Dr. Young and his group at MPFI study the molecular mechanisms regulating synaptic function. Understanding these mechanisms is critical because the major causes of brain diseases are due to synaptic dysfunction.

See more here:
Michael J. Fox Foundation grant to Dr. Samuel Young will provide Parkinson's drug development tools

Washington, May 3 : Researchers are developing a preventive therapy to halt symptoms in Parkinson's patients.

Parkinson's disease is characterized by a gradual loss of neurons that produce dopamine. Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson's symptoms at a young age.

The ability to modify the activity of DJ-1 could change the progress of the disease, said Dr. Nirit Lev, a researcher at Tel Aviv University's Sackler Faculty of Medicine and a movement disorders specialist at Rabin Medical Center.

Working in collaboration with Profs. Dani Offen and Eldad Melamed, Dr. Lev has now developed a peptide which mimics DJ-1's normal function, thereby protecting dopamine- producing neurons. What's more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.

Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain.

Dr. Lev said that this method could be developed as a preventative therapy.

As we age, we naturally lose dopamine-producing neurons. Parkinson's patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person.

Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson's patient or aging normally, said Dr. Lev.

The researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle.

'We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain,' explained Dr. Lev.

Continue reading here:
Soon, therapy to freeze Parkinson's in its tracks

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.

Continued here:
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.

The rest is here:
Once-Marginalized Parkinson's Disease Theory May Be Valid

ScienceDaily (May 2, 2012) Parkinson's disease, a disorder which affects movement and cognition, affects over a million Americans, including actor Michael J. Fox, who first brought it to the attention of many TV-watching Americans. It's characterized by a gradual loss of neurons that produce dopamine. Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson's symptoms at a young age.

The ability to modify the activity of DJ-1 could change the progress of the disease, says Dr. Nirit Lev, a researcher at Tel Aviv University's Sackler Faculty of Medicine and a movement disorders specialist at Rabin Medical Center. Working in collaboration with Profs. Dani Offen and Eldad Melamed, Dr. Lev has now developed a peptide which mimics DJ-1's normal function, thereby protecting dopamine-producing neurons. What's more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.

Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. Dr. Lev says that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.

Guarding dopamine levels

As we age, we naturally lose dopamine-producing neurons. Parkinson's patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson's patient or aging normally, says Dr. Lev.

The researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle. "We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain," explains Dr. Lev.

In pre-clinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson's disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.

Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this peptide does not. Additionally, it provides a safe treatment option because peptides are organic to the body itself.

Filling an urgent need

According to Dr. Lev, this peptide could fill a gap in the treatment of Parkinson's disease. "Current treatments are lacking because they can only address symptoms -- there is nothing that can change or halt the disease," she says. "Until now, we have lacked tools for neuroprotection."

See the article here:
Freezing Parkinson's in its tracks: Researcher developing therapy to halt symptoms in Parkinson's patients

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/c9kszn/parkinsons_diseas) has announced the addition of GlobalData 's new report "Parkinson's Disease Therapeutics - Global Drug Forecasts and Treatment Analysis to 2020" to their offering.

Parkinson's Disease (PD) Therapeutics Market is Forecast to Show Slow Growth to 2020

In 2011, the global Parkinson's Disease (PD) therapeutics market, which includes the key markets of the US, Japan, Germany, the UK, France, Italy, Spain, Brazil, China, India and Russia was estimated to be worth $2,992m. During the period 2002-2011, the global PD therapeutics market grew at a Compound Annual Growth Rate (CAGR) of 5.8%. GlobalData analysis shows that the market size was primarily driven by two key parameters: the increase in PD prevalence due to the increase in the aging population in the 11 key markets and the increasing cost of therapy.

In 2011, the market registered a decline in the market valuations due to the entry of generics for Mirapex (pramipexole) and higher preference for generic ropinirole. The market declined from $3,499m in 2010 to $2,992m in 2011. The US was leading PD therapeutics market, with an estimated value of $1,046m in 2011 and a market share of 35%. Japan was the second biggest market, with an estimated value of $542m and an 18.1% market share, followed by Germany with a market share of 15.6%.

The global PD therapeutics market is primarily served by levodopa, dopamine agonists, Monoamine Oxidase Inhibitors (MAO-BI) and Catechol-O-Methyltransferase (COMT) inhibitors. The market is dominated by branded products such as Boehringer Ingelheim's Mirapex/Mirapexin / Sifrol / Mirapex ER / Mirapexin ER (pramipexole), GlaxoSmithKline's (GSK) Requip/Requip XL (ropinirole), Orion / Novartis' Stalevo/Comtan (carbidopa/levodopa/entacapone) and Teva/Lundbeck's Azilect/Agilect (rasagiline). In addition, a large number of generics are also available in this market.

Key Topics Covered:

1 List of Tables and Figures

2 Parkinson's Disease Therapeutics - Disease Overview

3 Parkinson's Disease Therapeutics - Market Characterization

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Research and Markets: Parkinson's Disease Therapeutics - Parkinson's Disease (PD) Therapeutics Market is Forecast to ...

Tried to pretend nothing was wrong ... Sonia Rykiel.

Sonia Rykiel has revealed she has Parkinson's disease, after finding it impossible to keep secret any longer.

The French fashion designer's health has been called into question over recent months, with claims she has been looking frail.

She made the announcement about her health in a new book called N'oubliez pas que je joue (Don't forget it's a game). The tome is co-written by Judith Perrignon and in it Rykiel talks about the disease.

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"Unfashion" ... Malin Akerman wears a Sonia Rykiel dress from the designer's autumn 2011 collection.

"I don't want to show my pain. I resisted, I hesitated, I tried to be invisible, to pretend that nothing was wrong. It's impossible, it's not like me," she says in the book.

The 81-year-old designer discovered she had Parkinson's 15 years ago. She has opened up about it now because she can no longer disguise the signs, such as shaking.

The star has been using a cane for a while now, although those she works with suggested she was never pictured with it.

Rykiel discussed her love of fashion in the latest edition of French Elle. She thinks women get too caught up in trends, when really they need to think about what suits their figures when getting dressed.

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Sonia Rykiel reveals Parkinson's disease

Thursday, Apr 26 2012, 4:34 pm

What is Parkinsons disease?

According to the Parkinsons Disease Foundation, Parkinsons is a chronic and progressive movement disorder that involves the malfunction and death of vital nerve cells in the brain, called neurons. Major symptoms are tremor, rigidity, slowness and lack of balance. Some of the other symptoms are depression, emotional changes, pain, memory loss, problems swallowing and chewing, digestive issues, sleep disturbances, fatigue and weight loss.

More information

The monthly Parkinsons Support Group meets at the Neal Senior Center, 100 T.R. Harris Drive, Shelby, at 1:30 p.m. on the second Tuesday of the month. Contact Doug Murphy at 704-487-8822 and dmurphy2@carolina.rr.com.

The quarterly Parkinsons Support Group will meet at 6 p.m. May 22 at the Life Enrichment Center, 110 Life Enrichment Blvd., Shelby. The program will be about the importance of exercise. For more information, call 704-484-0405.

Online

Parkinsons Disease Foundation: http://www.pdf.org/, 1-800-457-6676

Parkinson Association of the Carolinas: http://www.parkinsonassociation.org, 1-866-903-7275

Mention Parkinsons and most people think of tremors, said Doug Murphy, who was diagnosed with the disease in 2009.

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Parkinson's is 'a daily struggle'

CHARLOTTE, N.C., April 25, 2012 (GLOBE NEWSWIRE) -- Chelsea Therapeutics International, Ltd. (CHTP - News) announced today it is proud to serve as a platinum corporate sponsor of the Parkinson's Unity Walk in New York City on April 28, 2012. In addition to sponsoring the walk, Chelsea employees will also participate in the event and raise funds for Parkinson's research.

"As a sponsor of the Parkinson's Unity Walk, Chelsea is helping to fund potentially life-saving research for this devastating disease," commented Dr. Simon Pedder, president and CEO of Chelsea Therapeutics. "Chelsea is committed to helping those with a wide range of autonomic conditions, including Parkinson's disease and Neurogenic OH. We are thrilled to be raising money to support seven of the nation's largest Parkinson's organizations and their premier fundraising event."

The Parkinson's Unity Walk (PUW), a grassroots organization, began in 1994 through the dedicated efforts of patients, families, support groups, and friends who were affected by Parkinson's disease. Their main goal was to raise awareness and funds for research to find a cure for Parkinson's. The Parkinson's Unity Walk directs donated funds to increase research to find a cure. 100% of all donations made to the Parkinson's Unity Walk are distributed among the major U.S. Parkinson's disease foundations for Parkinson's disease research including the American Parkinson Disease Association, the National Parkinson Foundation, the Parkinson's Action Network, the Parkinson's Disease Foundation, The Michael J. Fox Foundation for Parkinson's Research, The Parkinson Alliance and The Parkinson's Institute and Clinical Center. To join a team, make a donation or learn more about the Parkinson's Unity Walk, please visit http://www.unitywalk.org.

About Chelsea Therapeutics

Chelsea Therapeutics (CHTP - News) is a biopharmaceutical development company that acquires and develops innovative products for the treatment of a variety of human diseases, including central nervous system, rheumatoid arthritis, psoriasis and other inflammatory diseases. Founded in 2004 around its library of unique anti-inflammatory and autoimmune technology, Chelsea has further expanded its product development portfolio with early- and late-stage candidates that seek to leverage the company's development expertise and accelerate the company's drug commercialization efforts. For more information about the company, visit http://www.chelseatherapeutics.com.

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Chelsea Therapeutics is a Proud Sponsor of the Parkinson's Unity Walk