Amyotrophic lateral sclerosis (ALS) 2016: Ice bucket challenge funds gene discovery, Parkinson’s disease, and BMI

By: Bel Marra Health
Saturday, July 30, 2016

Remember the Ice Bucket Challenge, the viral charity campaign bringing awareness to amyotrophic lateral sclerosis (ALS)? Well, we have some good news for you. The funds raised during this initiative helped scientists discover the genes responsible for ALS! The joined efforts of enthusiasts who poured over themselves a bucket of iced water soliciting donations for the research enabled the scientists to make an ALS breakthrough, which hopefully will bring us steps closer to understanding the disease and improving treatments.

In light of these news, here are some of our articles discussing ALS, along with associated health issues, such as BMI, alcohol consumption, and Parkinson’s disease.

Parkinson’s disease vs. ALS, differences in symptoms, causes, and treatment

Parkinson’s disease and ALS can cause difficulties in movement and are both known to be progressive neurological diseases.

ALS is part of a cluster of disorders known as motor neuron diseases that involve gradual degeneration and death of motor neurons. In a healthy individual, messages from motor neurons in the brain are transmitted to the motor neurons in the spinal cord and sent to the particular muscles. In ALS, this communication degenerates and cells begin to die. As a result, the message that is transmitted is incomplete. Unable to function, the muscles begin to weaken and waste away over time. Eventually, communication from the brain to muscles is lost completely.

In its early stage, ALS – also known as Lou Gehrig’s disease – may appear as Parkinson’s disease, which is also a neurological disease similar to ALS. Here we will outline the causes, symptoms, and treatment options for both ALS and Parkinson’s disease to help you understand the differences between the two

Parkinson’s disease and ALS can cause difficulties in movement and are both known to be progressive neurological diseases.

ALS is part of a cluster of disorders known as motor neuron diseases that involve gradual degeneration and death of motor neurons. In a healthy individual, messages from motor neurons in the brain are transmitted to the motor neurons in the spinal cord and sent to the particular muscles. In ALS, this communication degenerates and cells begin to die. As a result, the message that is transmitted is incomplete. Unable to function, the muscles begin to weaken and waste away over time. Eventually, communication from the brain to muscles is lost completely.

In its early stage, ALS – also known as Lou Gehrig’s disease – may appear as Parkinson’s disease, which is also a neurological disease similar to ALS. Here we will outline the causes, symptoms, and treatment options for both ALS and Parkinson’s disease to help you understand the differences between the two.

Parkinson’s disease vs. ALS: U.S. prevalence

One million Americans live with Parkinson’s disease. The average cost of Parkinson’s disease including treatment, lost work wages, and social security payments is $25 billion annually in the U.S.

It is not clear how many people are affected by ALS, but the estimates range between 12,000 and 15,000. Doctors tell roughly 5,000 patients annually that they have ALS. Records on ALS have not been well kept across the country, so estimates may fall way below the actual rates. Common age of ALS diagnosis is between 55 and 75, and life expectancy is anywhere between two and five years after the onset of symptoms. Longevity in ALS is strongly linked to a person’s age. Younger individuals with ALS tend to live longer than those diagnosed at an older age.

Link between Parkinson’s disease and ALS

Parkinson’s disease and ALS are a lot more similar than you may think. The two neurological diseases share neurons that are highly sensitive to stress, misfolded proteins and reduced protein recycling, toxic proteins that spread from neuron to neuron, and neuroinflammation which is triggered by the immune system and aggravates the condition.

These commonalities between ALS and Parkinson’s disease allow researchers to better hone in on more effective treatments for both diseases.

Difference between Parkinson’s disease and ALS signs and symptoms

Parkinson’s disease typically begins with tremors, followed by muscle stiffness, difficulty standing or walking, changes in speech, slow movements, impaired posture and balance, loss of automatic movements, and writing changes.

Signs and symptoms of ALS include slurred speech, hoarseness, difficulty swallowing, emotional liability (involuntary laughing or crying), loss of tongue muscle contour, excess saliva, difficulty breathing, limp muscles or flaccid weakness, muscle wasting, and twitching.

In the early stages of the disease, ALS patients may notice that performing regular everyday tasks has become more challenging. For example, they may experience difficulty climbing steps or getting up from a chair. Symptoms may first begin on one side of the body, but as the condition progresses, they spread to both sides.

As you can see, ALS and Parkinson’s disease share symptoms associated with the negative impact of both conditions on movement and muscle function.

Comparing Parkinson’s disease and ALS causes

When certain nerve cells in the brain begin to die or break down that is what causes Parkinson’s disease, but why this occurs is unclear. Some factors that contribute to nerve cell death include genetics as specific gene mutations have been identified to contribute to Parkinson’s disease, environmental factors such as exposure to certain toxins, the presence of Lewy bodies in the brain, as well as alpha-synuclein found in Lewy bodies.

There are many unanswered questions about ALS, including the root cause. What we do know is that nerve cells that control the movement of muscles gradually die in ALS patients.

Researchers around the world continue to investigate the possible causes of ALS, including whether the immune system plays a role in attacking the body cells, potentially killing nerve cells. Scientists are examining chemical imbalance and trying to determine if proteins in people with ALS are being incorrectly processed by nerve cells.

Environmental factors are also being put under the scrutiny. One study has stated that members of the military personnel in the Gulf region during the 1991 war were more likely to develop Lou Gehrig’s disease than military personnel stationed anywhere else. The question is, could mechanical or electrical trauma, exposure to high levels of exercise, exposure to high levels of agricultural chemicals, or heavy metals play a role?

Parkinson’s disease vs. ALS: Risk factors and complications

Risk factors for Parkinson’s disease include being over the age of 50, being male, having a family history of Parkinson’s disease, carrying gene variations, experiencing a head injury, being exposed to environmental toxins, and taking certain medications such as anti-anxiety medications or sleeping pills.

Complications associated with Parkinson’s disease include difficulty thinking, depression, emotional changes, swallowing problems, sleep problems and disorders, bladder issues, constipation, changes in blood pressure, smell dysfunction, fatigue, pain, and sexual dysfunction.

Studies into ALS have revealed some interesting insight. For example, it may just be that some people with this disease are triggered by certain environmental factors. The environmental triggers under investigation include smoking, lead exposure, and military service. Recent research has indicated that people who have served in the military are at a higher risk of getting ALS.

Studies are also looking at the entire human genome, since research has uncovered a number of genetic variations that people with familial ALS and some with non-inherited ALS have in common. These variations might make people more prone to ALS.

While muscle control and speech problems are earlier signs of ALS, complications arise and include paralysis and difficulty breathing. Some people use ventilation machines to assist them in breathing, and others choose to have a tracheostomy, which is a hole created at the front of their neck leading into their windpipe to allow for the use of a respirator to inflate and deflate their lungs. Respiratory failure is the most common cause of death for people who are diagnosed with ALS.

Difference in Parkinson’s disease and ALS diagnosis and treatment

There is currently no specific test that can be performed to directly diagnose Parkinson’s disease, but an array of different tests can help narrow down on a diagnosis. If Parkinson’s disease is suspected, a patient will be referred to a neurologist and geriatrician. Diagnosis is commonly confirmed with the presence of at least two of the three most common symptoms: Shaking or tremor that occurs at rest, slowness of movement, and muscle stiffness. A doctor will also perform brain scans to diagnose Parkinson’s disease and to check for other conditions that could be causing similar symptoms.

There is also no cure for Parkinson’s disease, but treatments are available to manage the symptoms and slow down the disease progression. Alongside traditional treatments, supportive therapies are used to improve different aspects of a person’s health.

Common medications prescribed in Parkinson’s disease include dopamine replacement therapy, dopamine agonists, anticholinergics, amantadine, monomine oxidase type B inhibitors, and catechol-o-methyl transferase inhibitors.

Surgery is also a treatment option for Parkinson’s disease and is best suited for those who had a good response to levodopa, but still have difficulties with movement or who experience large fluctuations in their levodopa levels.

Supportive therapies for Parkinson’s disease include physical therapy to improve movement, occupational therapy, speech and language therapy, and diet modifications such as increasing fiber and salt intake, eating frequently but in smaller portions, and adjusting the diet to prevent unintentional weight loss.

ALS is very hard to diagnose because – like with Parkinson’s disease – no specific test has been established to determine if a person has this fatal condition. A clinical examination, diagnostic tests, and often ruling out other diseases can help a doctor identify the problem. Diagnostic tests may include blood and urine tests, a spinal tap, X-rays, an MRI, an EMG, or even a muscle or nerve biopsy. A thorough neurological examination is also a diagnostic measurement.

Since there is no cure for ALS, the treatment focuses on helping the patient cope with the symptoms, preventing unnecessary complications, as well as slowing the progress of the disease. There is an FDA-approved drug (Riluzole) that has slowed the progression of ALS is some people. Doctors also prescribe various medications to treat the many symptoms of the disease.

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Sources:
http://www.nhs.uk/Conditions/Parkinsons-disease/Pages/Diagnosis.aspx
http://www.alsa.org/about-als/aam-2014/learn-about-als/common-threads.html

http://www.belmarrahealth.com/amyotrophic-lateral-sclerosis-als-2016-ice-bucket-challenge-funds-gene-discovery-parkinsons-disease-and-bmi/

Study of gene mutations improves understanding of inherited Parkinson’s disease

July 29, 2016

Scientists have developed a new method of measuring the activity of disease-causing mutations in the LRRK2 gene, a major cause of inherited Parkinson’s disease.

The team believes this breakthrough, which was published in the Biochemical Journal, could expedite future development of a clinical test that could facilitate the evaluation of drugs to target inherited Parkinson’s disease.

“It’s important to better understand how disruption in LRRK2 biology causes Parkinson’s disease and whether a drug that targeted the LRRK2 enzyme would offer therapeutic benefit,” said lead study author Professor Dario Alessi from the University of Dundee.

Mutations in the LRRK2 gene are the most common cause of genetic Parkinson’s disease (~1% total cases). The most common disease-causing mutation in this gene increases the activity of the LRRK2 protein (enzyme) three-fold, which implies that the increase in activity of the protein may contribute towards the symptoms of the disease in these patients. It also suggests that drugs that reduce the activity of the LRRK2 protein (LRRK2 inhibitors) may help treat patients with this form of inherited Parkinson’s disease.

“Current drug treatments only deal with symptoms of the condition, such as tremors, but do not affect the progression of Parkinson’s disease. An important question is whether a LRRK2 therapy might have potential to slow progression of the condition, which no other current therapy is able to do,” commented Alessi.“

When the LRRK2 protein is active it stops another cellular protein called Rab10 from fulfilling its function in the body. There are many proteins in the Rab family and a number of them have been shown to be low in number or deactivated in different forms of Parkinson’s disease. The new method, which was developed using a mouse model, was established by a collaboration of researchers from the University of Dundee, The Michael J. Fox Foundation for Parkinson’s Research, GSK and the University of Hong Kong. 

“The prediction is that elevation of LRRK2 activity leads to Parkinson’s disease, and this is now testable using our assay,” said Alessi. “The expectation is that if a sub-group of patients can be identified with elevated LRRK2 activity, these individuals might benefit most from LRRK2 inhibitors.”

New assay promising for inherited Parkinson’s research

This new experimental assay is straightforward; only requires small amounts of sample material; and is suitable for adapting to analyse large samples. This is in contrast to current mass spectrometry technology that is more complex and cumbersome and requires larger sample sizes.

While acknowledging that more work is needed, the researchers believe this breakthrough could help with future drug developments for patients with this form of Parkinson’s disease.

“I am hopeful that the new technology [utilised] in our study will greatly aide future work on defining the role that LRRK2 plays in Parkinson’s disease. I am also particularly excited about the potential of the methodology we have elaborated, especially if it could be exploited to assess LRRK2 activity in Parkinson’s patients and accelerate development and evaluation of LRRK2 drug candidates,” Alessi explained

A commentary by Dr Patrick Eyers, University of Liverpool, accompanying the research paper will be published later this month in the same journal.

http://www.drugtargetreview.com/13343/content-type/industry-news/study-inherited-parkinsons/

Scientists Cultivate Midbrain-like Organoids to Research Parkinson's Disease

July 29, 2016

Anchor: A research team led by South Korean and Singaporean scientists says it successfully cultivated midbrain-like organoids using human embryonic stem cells for the first time in the world. The scientists have expressed hope that their study will find a way to treat Parkinson's disease. Our Bae Joo-yon has more. 

Report: An international team of researchers led by South Korean and Singaporean scientists says it succeeded, for the first time in the world, in cultivating midbrain-like organoids using human embryonic stem cells.

 

Professor Je Hyun-soo of Duke-National University of Singapore Medical School said Friday that the organoids, which are miniature organs in vitro, were jointly cultivated with a group of researchers at the Genome Institute of Singapore. 

The cultivated organoids are around two millimeters in size, or similar to the size of the midbrain of a fetus during the second trimester. They are about a quarter of the entire brain size of lab mice.

 

Professor Je and Huck-Hui Ng, head of the Genome Institute of Singapore, said that their team developed a 3D organoid model of the midbrain with the aim of finding a way to treat Parkinson’s disease, adding the model will likely overcome the limits of animal testing.

 

Je said that with the midbrain-like organoids, the growth of brain tissues can be continuously observed and could shed light on what causes Parkinson’s disease and how the progressive neurological disorder works.

 

Located at the very center of the brain, the midbrain is associated with vision, hearing and motor control.

 

The research team also discovered that the midbrain-like organoids produce neuromelanin, which is a key pigment found in substantia nigra which is closely linked to Parkinson’s disease.

 

The team’s research results were published in the journal Cell Stem Cell, on Thursday.

Bae Joo-yon, KBS World Radio News.

http://world.kbs.co.kr/english/news/news_Sc_detail.htm?No=120750

Parkinson’s could be slowed by new drugs if research on gene-tracking pays off

July 29, 2016

There is no cure for the condition and doctors are only able to treat the symptoms, which include tremors, slow movement and stiff muscles

A new generation of Parkinson’s drugs could be on the way

Tracking the genetic mutations that cause Parkinson’s could lead to drugs which slow the disease, experts say. 

Currently there is no cure for the progressive neurological condition affecting 127,000 Britons – one in 500.

It sees parts of the brain become progressively damaged over many years. The three main symptoms are involuntary shaking of particular parts of the body, slow movement and stiff and inflexible muscles.

Doctors have only been able to treat symptoms but cannot stop, or slow its advance. 

But a new way of measuring the activity of mutations in the LRRK2 gene, a major cause of inherited Parkinson’s, brings fresh hope of early diagnosis and breakthrough treatments.

Symptoms include tremors

Prof Dario Alessi of the University of Dundee, whose study was published in the Biochemical Journal, said it has “potential to slow progression” of the disease.

More research is needed but the breakthrough, funded by the Michael J. Fox Foundation among others, could help with future drug developments.

Professor Aideen Sullivan from University College Cork said: “If this method can be applied to human samples, it will be a significant step toward earlier and more definitive diagnosis of Parkinson’s, a disease of steadily increasing prevalence that currently affects over 10 million people worldwide.”

The study was published in the Biochemical Journal.

http://www.mirror.co.uk/lifestyle/health/parkinsons-could-slowed-new-drugs-8524277?

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UAB researchers uncover vital mechanism for L-DOPA-induced-dyskinesia

July 29, 2016

Though the drug levodopa can dramatically improve Parkinson's disease symptoms, within five years one-half of the patients using L-DOPA develop an irreversible condition -- involuntary repetitive, rapid and jerky movements. This abnormal motor behavior appears only while taking L-DOPA, and it stops if the drug is stopped. However, if L-DOPA is taken again, even many months later, it quickly re-emerges.

In research to prevent this side effect and extend the usefulness of L-DOPA -- which is the most effective drug treatment for Parkinson's disease -- University of Alabama at Birmingham researchers have uncovered an essential mechanism of this long-term memory for L-DOPA-induced-dyskinesia, or LID.

They report a widespread reorganization of DNA methylation -- a process in which the function of DNA is modified -- in brain cells caused by L-DOPA. They also found that treatments that increase or decrease DNA methylation can alter dyskinesia symptoms in an animal model.

Thus, modification of DNA methylation may be a novel therapeutic target to prevent or reverse LID behavior.

"L-DOPA is a very valuable treatment for Parkinson's, but in many patients its use is limited by dyskinesia," said David Standaert, M.D., Ph.D., the John N. Whitaker Professor and chair of the Department of Neurology at UAB. "Better means of preventing or reversing LID could greatly extend the use of L-DOPA without inducing intolerable side effects. The treatments we have used here, methionine supplementation or RG-108, are not practical for human use; but they point to the opportunity to develop methylation-based epigenetic therapeutics in Parkinson's disease."

The research by David Figge, Karen Eskow Jaunarajs, Ph.D., and corresponding author David Standaert, Center for Neurodegeneration and Experimental Therapeutics, UAB Department of Neurology, was recently published in The Journal of Neuroscience.

Research Details 

Although studies of LID in animal models have shown changes in gene expression and cell signaling, a key unanswered question still remained: Why is the neural sensitization seen in LID persistent when delivery of L-DOPA is transient?

The UAB researchers suspected DNA methylation changes -- the attachment of a methyl group onto nucleotides in DNA -- because methylation is known to stably alter gene expression in cells as they grow and differentiate. Furthermore, methylation changes in neurons have been shown to be involved during the formation of place memory and the development of addictive behavior after cocaine use.

In general, increased DNA methylation has a silencing effect on nearby gene expression, while removal of the methyl groups enhances gene expression.

Figge and colleagues found that:

• L-DOPA treatment of parkinsonian rodents enhanced the expression of two DNA demethylases.
• Cells in the dorsal striatum in the LID model showed extensive, location-specific changes in DNA methylation, mostly seen as demethylation.
• The changes in DNA methylation were near many genes with established functional importance in LID.
• Modulating global DNA methylation -- either by injecting methionine to increase methylation or applying RG-108, an inhibitor of methylation, to the striatum -- modified the dyskinetic behavior of LID, down or up, respectively.

"Together," the researchers wrote, "these findings demonstrate that L-DOPA induces widespread changes to striatal DNA methylation and that these modifications are required for the development and maintenance of LID."

Source:

University of Alabama at Birmingham

http://www.news-medical.net/news/20160729/UAB-researchers-uncover-vital-mechanism-for-L-DOPA-induced-dyskinesia.aspx?

Parkinson's Fundraiser Nets $50,000, Draws Tori Spelling, Jason Priestley and Tiffani Thiessen

JULY 28, 2016

Wendi McLendon-Covey arrives at the Raising The Bar To End Parkinson's fundraiser at Laurel Point in Studio City on July 27, 2016. (Photo by Greg Doherty/Getty Images)

The annual event, in partnership with The Michael J. Fox Foundation, took over the about-to-open seafood restaurant Laurel Point. But Fox's onetime costar Betsy Brandt had more than food on the brain: "If you're going to donate to a charity, this is a great charity because the way they put your money to use is so effective."

Married actors Steve Howey and Sarah Shahi catch up with actor Brady Smith at the Raising The Bar To End Parkinson's fundraiser at Laurel Point in Studio City on July 27, 2016. (Photo by Greg Doherty/Getty Images)

Wendi McLendon-Covey has never met Michael J. Fox, but she shows up for him — even when he's not around. 

The actress and star of ABC's The Goldbergs stood alongside actors Betsy Brandt, Missi Pyle, Amanda Crew, Dustin Milligan and June Diane Raphael as part of the honorary committee for Wednesday night's Raising the Bar to End Parkinson's fundraiser in partnership with The Michael J. Fox Foundation. And she told The Hollywood Reporter that her appearance at the Studio City event — held at not-yet-opened restaurant Laurel Point on Ventura Boulevard — was way more than a typical step-and-repeat opportunity. This was personal. 

"My dad has Parkinson's and my husband has it, too," said the actress, who has been married to Greg Covey since 1996. "So I'm all about the Michael J. Fox Foundation. My dad has gotten a lot of resources from the foundation. When he was diagnosed two years ago, he went to the website and followed all the leads and it helped him contradict what his doctors were telling him as they weren't being as proactive as they should've been. This foundation has given so much to my family that when they asked me to get involved, I said, 'Hell yes!' I'm happy to be involved in any way I can."  

Tori Spelling, UTA's Jacob Fenton and Tiffani Thiessen attend the Raising The Bar To End Parkinson's fundraiser at Laurel Point in Studio City on July 27, 2016. (Photo by Greg Doherty/Getty Images) 

McLendon-Covey wasn't the only one on the red carpet who has been affected by the chronic disorder which affects the central nervous system and counts more than 1 million cases in the U.S. currently. Actor Grant Show told THR that his late father, who passed away three years ago, was afflicted with Parkinson's. "It's a tough disease — there are no answers to it," he said. 

Organizers would likely counter Show's statement and say that the solution is raising money to help scientists and researchers find for a cure. And on that note, Wednesday night's exclusive peek inside Laurel Point, a new seafood and sushi concept restaurant from executive chef Phil Kastel (Public School, The Grill on the Alley), proved to be a success with more than $50,000 raised from a raffle and silent auction. 

"If you're going to donate to a charity, this is a great charity because the way they put your money to use is so effective," praised Brandt, who starred opposite Fox on his The Michael J. Fox Show playing his wife. "If we're going to cure this disease, it's going to be because of this foundation." 

Jason Priestley also had nice words to say about his fellow Canadian pal Fox. "I've had the good fortune of being friends with Mike for some time," said Priestley, who now stars on a popular Canadian series Private Eyes. "And I so admire him as a man for the way in which he dealt with this disease and how he formed this foundation to fight it and try to help other people." 

Speaking of other people, Priestley spent part of the party catching up with his onetime Beverly Hills 90210 costar Tori Spelling, who attended the event with husband Dean McDermott. The two posed for photos but skipped interviews on the press line, instead heading straight inside the bash where they caught up with fellow attendees like Tiffani Thiessen, Minka Kelly, Naya Rivera, Ryan Dorsey, Josh Radnor, Steve Howey, Sarah Shahi, Chelsea Kane, Josh Peck, Hunter Parrish and Jake McDorman. Fox's Back to the Future costar Lea Thompson also made the rounds.

Though THR never spotted her drinking one of the night's speciality cocktails, it's possible the actress sipped on one of two exclusive drinks created by mixologist Danny Natali: the Teen Wolf Summer with Corralejo Tequila Blanco, cilantro and lime, and the Save the Clock Tower with Three Olives Vodka, watermelon, mint and lime. Food options included on K-Town crispy chicken sidekicks, seasonal oysters with yuzu kosho mignonette, crab deviled eggs with smoked roe, crab and hamachi rolls, and chocolate tars with maldon sea salt. The general public can sample the menu when the restaurant officially opens on Aug. 1.

The packed room and the attendees' generosity made Veronique Enos Kaefer, director of advancement for The Michael J. Fox Foundation, catch her breath. "The people who are on this committee, they reach out and the whole community comes together and they raise a ton of money and it all goes to research," she said. "We couldn't be more grateful."

Lea Thompson arrives at the Raising The Bar To End Parkinson's event at Laurel Point in Studio City on July 27, 2016. (Photo by Amanda Edwards/WireImage)

Many of those in attendance also said they were feeling grateful, too, but theirs was directed at UTA agent Jacob Fenton, who is married to Kastel. He helped with the heavy lifting for the event, inviting many of his clients and industry friends on behalf of the foundation and its efforts in finding a cure. 

And while they do that, McLendon-Covey said that she and her family will continue to lean on the efforts of Fox and friends. "You can't mend this thing, but you can manage it."

http://health.einnews.com/article/337384842/6mQJscpdIG8wg_PU

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Michael J. Fox Foundation Vice President Of Medical Communications Joins Alliance For Patient Access Meeting

NEW YORK, July 29, 2016 

Today, Rachel Dolhun, MD, vice president of medical communications at The Michael J. Fox Foundation for Parkinson's Research (MJFF), will join a coalition of physicians for the inaugural meeting of the Physicians Neurodegenerative Disease Working Group in Washington, D.C. The group will discuss issues impacting patient access to medical therapies and recommend educational resources and advocacy initiatives with the goal of informing policymaking around breakthrough therapies for neurodegenerative diseases, including Parkinson's disease (PD).

The recently established Physicians Neurodegenerative Disease Working Group is organized by the Alliance for Patient Access (AfPA), a national network of physicians dedicated to ensuring patient access to approved therapies and appropriate clinical care. The working group aims to address a number of barriers to access, including high out-of-pocket costs and insurance restrictions. To advocate for patients with PD, Dr. Dolhun draws on her previous clinical experience as a movement disorder specialist as well as her current work in communications at MJFF.

Parkinson's disease affects one million people in the United States. No disease-modifying therapy has yet been proven, but a number of potential drugs are in development. New symptomatic treatments for both motor and non-motor symptoms have recently reached market and many more are in late stages of clinical trials. While working aggressively to accelerate therapeutic development, MJFF is concurrently supporting Parkinson's public policy efforts to reduce challenges to patients' access to care and new therapies. Dr. Dolhun's participation in the AfPA conference represents MJFF's commitment to these endeavors.  

Learn more about the Foundation's work to speed a cure for PD at michaeljfox.org.

About The Michael J. Fox Foundation for Parkinson's Research

As the world's largest nonprofit funder of Parkinson's research, The Michael J. Fox Foundation is dedicated to accelerating a cure for Parkinson's disease and improved therapies for those living with the condition today. The Foundation pursues its goals through an aggressively funded, highly targeted research program coupled with active global engagement of scientists, Parkinson's patients, industry leaders, government research funders and regulators, clinical trial participants, donors and volunteers. In addition to funding more than $600 million in research to date, the Foundation has fundamentally altered the trajectory of progress toward a cure. The Foundation increases the flow of participants into Parkinson's disease clinical trials with its online tools Fox Trial Finder and Fox Insight; sponsors a landmark, international study to find reliable and consistent biomarkers of Parkinson's progression; promotes Parkinson's awareness through high-profile events and outreach; advocates for state and federal policies that support medical research and increased access to health care; and coordinates the involvement of thousands of Team Fox members and grassroots volunteers around the world.

For more information, visit www.michaeljfox.org.

http://www.prnewswire.com/news-releases/michael-j-fox-foundation-vice-president-of-medical-communications-joins-alliance-for-patient-access-meeting-300306052.html?