Finding Points to Possible Mechanism Underpinning Alzheimer's and Parkinson's

Thursday February 12, 2015

Medical Xpress - Scientists from the Florida campus of The Scripps Research Institute (TSRI) have for the first time discovered a killing mechanism that could underpin a range of the most intractable neurodegenerative diseases such as Alzheimer's, Parkinson's and ALS.

The new study, published recently in the journal Brain, revealed the mechanism of toxicity of a misfolded form of the protein that underlies prion diseases, such as bovine spongiform encephalopathy ("mad cow disease") and its human equivalent, Creutzfeldt-Jakob disease.

"Our study reveals a novel mechanism of neuronal death involved in a neurodegenerative protein-misfolding disease," said Corinne Lasmézas, a TSRI professor who led the study. "Importantly, the death of these cells is preventable. In our study, ailing neurons in culture and in an animal model were completely rescued by treatment, despite the continued presence of the toxic misfolded protein. This work suggests treatment strategies for prion diseases—and possibly other protein misfolding diseases such as Alzheimer's."

Failure and Rescue of Brain Cells

In the new study, the scientists used a misfolded form of the prion disease protein, called TPrP, a model they had previously developed, to study misfolded protein-induced neurodegeneration in the laboratory. Misfolded proteins are the common cause of the group of diseases comprising prion, Alzheimer's, Parkinson's diseases, ALS and other conditions.

Using biochemical techniques, the researchers demonstrated that TPrP induces neuronal death by profoundly depleting NAD+ (nicotinamide adenine dinucleotide)—a metabolite well known as a coenzyme that is common to all cells and necessary for energy production and cellular homeostasis.

Restoring NAD+ proved to be the critical factor for the rescue of neurons subjected to TPrP injury. Even when added three days after TPrP exposure, an infusion of NAD+ reversed within only a few hours the fate of neurons that had been doomed to destruction.

"Our study shows for the first time that a failure of NAD+ metabolism is the cause of neuronal loss following exposure to a misfolded protein," Lasmézas said.

The loss of NAD+ also triggers autophagy—a way cells rid themselves of damaged material such as misfolded proteins—and apoptosis, or programmed cell death, the last resort of the cell when everything starts to go wrong. However, the researchers demonstrated these mechanisms do not initiate the neuronal demise.

"We show that apoptosis or programmed cell death and autophagy are not primary players in the death cascade," said Staff Scientist Minghai Zhou, the first author of the study. "Modulation of neither of these processes significantly alters the death of TPrP-exposed neurons. This is all caused by NAD+ disappearing—the cell cannot survive without it."

Lasmézas noted the loss of NAD+ is suggestive of some other neurodegenerative diseases, such as Parkinson's where NAD+ depletion could play a role in mitochondrial failure.

New Grant to Support Further Research

A recent $1.4-million grant from the National Institute of Neurological Disorders and Stroke (NINDS) will support further work to look for drug candidates based on the new findings.

Lasmézas and Louis Scampavia, a TSRI associate professor of molecular therapeutics, will be co-principal investigators for the new three-year study, whose team will also include Tom Bannister, a TSRI associate scientific director at Scripps Florida's Translational Research Institute.

The scientists have developed several primary tests for compounds that could restore NAD+ and plan to begin those tests at Scripps Florida's High Throughput Screening facility.

Since it was established in 2005, the Scripps Florida High Throughput Screening facility has screened more than 200 targets in more than 235 industrial and academic collaborations—several of these collaborations have produced successful clinical trial candidates. The drug discovery facility is currently capable of routinely screens one quarter of a million compounds in a single day.

http://medicalxpress.com/news/2015-02-mechanism-underpinning-alzheimer-parkinson-diseases.html

APDM MOBILITY LAB FOR PARKINSON'S DISEASE ASSESSMENT

11th February 2015 - New research

The diagnosis and estimation of disease severity in Parkinson's Disease was assessed using the APDM Mobility Lab. The APDM Mobility Lab uses wearable sensors and sophisticated signal processing to track even subtle changes in gait, stride, balance, rotation, and efficiency and range of movement in upper and lower limbs and torsos. Sensors are simply strapped on to the subject on various parts of the body, including the chest, waist, wrists and ankles. Subjects perform a standardised test and then a report is generated. For more information go to : http://apdm.com/gait-and-posture/Mobility-Lab/
Each person performed iTUG (instrumented Timed-Up- and-Go) and iSway (instrumented Sway) using the APDM Mobility Lab. They were assessed according to a range of Parkinson's Disease scores. iTUG and iSway variables differentiated people with Parkinson's Disease from people who did not. They correlated with all Parkinson's Disease severity measures. Objective scores correlated more strongly with iTUG than iSway.
The study identified sets of iTUG and iSway variables that correlate with Parkinson's Disease severity measures and differentiate people with Parkinson's Disease. The authors suggest that these gait and balance measures could therefore potentially serve as markers of Parkinson's Disease progression. They are consequently under evaluation for this purpose in the ongoing NIH Parkinson Disease Biomarker Program.

Reference : Journal of Neurological Science [2014] 345 (1-2) : 131-138 (D.C.Dewey, S. Miocinovic, I.Bernstein, P.Khemani, R.B.Dewey, R.Querry, S.Chitnis, R.B.Dewey Jr) Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/25082782
http://www.viartis.net/parkinsons.disease/news/150211.pdf mail@viartis.net
©2015 Viartis 

Breath test for Parkinson's disease

Experts believe that a simple breath test could help doctors detect and diagnose Parkinson's disease. 

The test looks for a unique signature of chemicals in exhaled breath.

Small studies in volunteers have begun and early findings suggest the test can identify those with the debilitating brain condition. 

Larger trials are now planned to see if it could truly be a useful test, particularly for picking up Parkinson's in its earliest stages.Currently, no test can conclusively show that a person has Parkinson's.

Instead, doctors reach a diagnosis based on a person's symptoms and test results - such as brain scans to rule out other diseases.

At this stage, Parkinson's may already be fairly advanced.

Identifying it earlier would be beneficial because it would mean treatment could be given sooner.

Sniff it out

Parkinson's disease is a progressive condition where there is gradual loss of nerve cells from the brain.

And it is thought that this degradation leaves a chemical footprint in the body that could potentially be used in diagnostic tests.

A scan showing tell-tale brain degeneration in a patient with Parkinson's

Scientists have been exploring different ways of finding such biomarkers, including looking in blood, spinal fluid, and exhaled breath. 

The breath test looks for traces of volatile organic compounds or VOCs in the air we exhale. 

In a small trial in Israel with 57 people, some with Parkinson's and some without, the test could identify the individuals with Parkinson's by looking for distinctive patterns of VOCs.

It also appeared to distinguish between different sub-types of the disease based on the presence and quantity of different VOCs.

The charity Parkinson's UK and experts at the University of Cambridge were intrigued by these early findings and are now setting out to do a bigger study involving 200 volunteers from England. 

Dr Simon Stott, who is part of this UK team and will be working alongside the scientists from the Israel Institute of Technology, in Haifa, said: "We would like to find biomarkers that can identify patients early. 

"A breath test would be really appealing because it's non-invasive, non-painful and can be done in seconds.

"While it wouldn't replace what doctors already do, it could be a useful diagnostic tool to help them."

The biggest hope is that there may be molecules in the breath of people with Parkinson's which throw up new options for drug targets. 

The researchers say they have many years of work ahead of them before they will know if the test can be used in clinics. 

Parkinson's disease

• One in 500 people in the UK has Parkinson's 
• A combination of genetic changes and environmental factors may be responsible for the condition
• There are different sub-types of the disease and they share the symptoms of tremor, muscle rigidity and slowness of movements.
• Start Quote
  A breath test would be really appealing because it's non-invasive, non-painful and can be done in seconds”
  Researcher Dr Simon Stott
  http://health.einnews.com/article/249260416/HMU80kgKXT3GZX_u

Creatine Doesn't Treat Parkinson's Disease, Study Says

TUESDAY Feb. 10, 2015, 2015 -- Creatine doesn't appear to slow the progression of Parkinson's disease, a new study finds.Creatine monohydrate is an amino acid believed to play an important role in energy production in cells, a process that may be impaired in people with Parkinson's disease. Previous research in mice suggested that creatine supplements might potentially protect nerve cells.

Parkinson's disease is a progressive disorder of the nervous system that causes tremors and affects movement, according to the Mayo Clinic.

The new study included more than 1,700 people in the United States and Canada who had been diagnosed with Parkinson's disease within the previous five years. All were receiving treatmentfor Parkinson's disease. As part of the study, they were randomly assigned to take creatine or a placebo in addition to their usual treatment.

The patients were enrolled from March 2007 to May 2010 and followed up until September 2013. The study was halted early because those taking creatine showed no differences in disease progression compared to those taking the placebo.

"These findings do not support the use of creatine monohydrate in patients with Parkinson's disease," study author Dr. Karl Kieburtz, of the University of Rochester, and colleagues wrote.

The study was published Feb. 10 in the Journal of the American Medical Association.

Parkinson's disease affects about 6 million people worldwide, including more than 500,000 Americans, according to the researchers.

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about Parkinson's disease.

http://www.drugs.com/news/creatine-doesn-t-parkinson-s-study-says-55581.html

Amarantus Announces Publication in BRAIN of Eltoprazine Phase 2a Clinical Study for Treating Parkinson's Disease Levodopa-Induced Dyskinesia

• Eltoprazine demonstrated significant beneficial anti-dyskinesia effect at 5 and 7.5 mg doses, with no reduction of levodopa efficacy 
• Eltoprazine was well tolerated at all dose levels, with no major adverse effects reported
• Results support advancing eltoprazine into Phase 2b chronic dosing, clinical studies, as a treatment for patients with Parkinson's disease levodopa-induced dyskinesia

SAN FRANCISCO and GENEVA, Feb. 10, 2015 (GLOBE NEWSWIRE) -- Amarantus BioSciences Holdings, Inc. (OTCQB:AMBS), a biotechnology company focused on developing diagnostics in neurology, and therapeutic products with the potential for orphan drug designation in the areas of neurology, psychiatry, ophthalmology and regenerative medicine, announced that the publication of the results of a Phase 2a study of eltoprazine in Parkinson's disease levodopa-induced dyskinesias (PD-LID). The paper titled, "Eltoprazine Counteracts L-DOPA-induced Dyskinesias in Parkinson's Disease: A Dose-Finding Study," has been published in Oxford Journals (Oxford University Press) online and will appear shortly in a future print edition of BRAIN - A Journal of Neurology.

Eltoprazine is a small-molecule 5-HT_1A/1B serotonin receptor agonist, investigational drug candidate, with a well-established safety profile. A Phase 2a dose-finding study was conducted with eltoprazine to determine its effect against levodopa-induced dyskinesia, in patients with Parkinson's disease (PD). The double-blind, randomized, placebo-controlled clinical study was led by Professor Per Svenningsson, M.D., Ph.D., Centre for Molecular Medicine, Karolinska Institutet, Professor Anders Björklund, Ph.D., Faculty of Medicine at Lund University, and Professor Håkan Widner, M.D., Ph.D., Faculty of Medicine at Lund University. The study was partially supported by a grant from The Michael J. Fox Foundation for Parkinson's Research.

Some researchers believe that, in the advanced stages of PD, as dopamine nerve terminals are lost, serotonergic terminals take up levodopa and convert it to dopamine instead. Unlike in dopamine nerve endings, the serotonin nerve terminals do not have a negative feedback loop, possibly causing an excessive release of dopamine and resulting in the development of abnormal involuntary hyperkinetic movements, known as levodopa-induced dyskinesias (LID). Pre-synaptic activation of serotonin receptors using a 5HT_1A/1B agonist may dampen this excessive dopamine release. In animal model studies of LID previously conducted in Professor Björklund's laboratory, simultaneous activation of 5-HT_1A and 5-HT_1B receptors was shown to effectively block LID. The Phase 2a dosing trial with eltoprazine was conducted as an initial clinical pharmacology study to determine if activation of 5-HT_1A/1Breceptors in Parkinson's disease subjects may replicate the effects of serotonin receptor activation seen in pre-clinical dyskinesia studies.

The study in 22 subjects with long standing PD-LID was a randomized, four-way crossover design in which patients received a single dose of placebo and eltoprazine, at 2.5, 5 and 7.5 mg, in combination with a challenge dose of levodopa (1.5 times usual dose), on four different days, separated by an interval of a week. Data from the study demonstrated that eltoprazine significantly reduced peak dose dyskinesia at both the 5 and 7.5 mg doses using the Combined Dyskinesia Rating Scale. The 5 mg dose also showed a significant anti-dyskinetic effect on other measures of dyskinesia, including the Rush dyskinesia rating scale. Importantly, there were no adverse effects on levodopa efficacy at any dose level as evidenced by United Parkinson's Disease Rating Scale (UPDRS Part III) observation. Additionally, all dose levels of eltoprazine were well tolerated with no major adverse effects reported.

"Eltoprazine's anti-dyskinetic effect is promising, especially given the reduction in dyskinesia following a levodopa challenge at one and a half times greater than the regular levodopa dose," said Charlotte Keywood, M.D., Chief Medical Officer at Amarantus. "Levodopa treatment is the current standard of care for patients to manage PD motor symptoms, despite the occurrence of dyskinesia with long-term use. Thus, we were very pleased to see that normal motor responses to levodopa, measured by UPDRS III, remained unchanged in all patients treated with eltoprazine."

The Phase 2a study also included a pharmacokinetic (PK) evaluation of eltoprazine. The data show that the PK characteristics of eltoprazine in PD patients are the same as those found in healthy subjects. Given the positive PK profile in PD patients and the acute anti-dyskinesia effect seen with the 5 and 7.5 mg doses, further advancement of eltoprazine into Phase 2b chronic dosing clinical studies to treat patients with PD-LID is warranted.

"We are pleased to have the eltoprazine study results published in this prestigious peer-reviewed journal," said Dr. Keywood. "The results of this proof of concept, first trial in PD-LID patients, support the findings of the non-clinical pharmacology studies conducted using animal models of PD-LID and show the predictive value of these models in aiding human drug development."

"The data from this study show an acute antidyskinetic effect of eltoprazine with no detriment to levodopa efficacy. With these data at hand, we are confident moving forward into longer-term dosing studies to further evaluate the utility of eltoprazine as a treatment for levodopa-induced dyskinesia," concluded Dr. Keywood.

Amarantus expects to file its Investigational New Drug Application (IND) with the U.S. Food and Drug Administration (FDA) and commence its Phase 2b study of eltoprazine in PD-LID subjects in the first quarter of 2015.

"Dyskinesia impacts quality of life of people with Parkinson's disease, and is therefore a top priority for the Foundation," commented Maurizio Facheris, M.D., M.Sc., Associate Director of research programs at The Michael J. Fox Foundation. "We are glad to see this project moving further through clinical testing and closer to patients' hands."

To access the online version of the paper titled, "Eltoprazine Counteracts L-DOPA-induced Dyskinesias in Parkinson's Disease: A Dose-Finding Study," please click here.

To access the Karolinska Institutet press release titled, "New therapeutic principle for Parkinsonian dyskinesia shows clinical effect," regarding the publication in BRAIN, please click here.

About Eltoprazine

Eltoprazine is a small molecule 5HT_1A/1B partial agonist in clinical development for the treatment of Parkinson's disease levodopa-induced dyskinesia (PD-LID) and Adult Attention Deficit Hyperactivity Disorder (ADHD). Eltoprazine has been evaluated in over 600 human subjects to date, and has a well-established safety profile. Eltoprazine was originally developed by Solvay Pharmaceuticals for the treatment of aggression. Upon Solvay's merger with Abbott Pharmaceuticals, the Eltoprazine program was out-licensed to PsychoGenics. PsychoGenics licensed Eltoprazine to Amarantus following successful proof-of-concept trials in PD-LID and adult ADHD.

About Parkinson's disease and levodopa-induced dyskinesia (PD-LID) 

Parkinson's disease is a chronic, progressive neurological disorder that causes motor symptoms such as tremors, rigidity and slowed movements as well as non-motor symptoms including cognitive impairment and autonomic dysfunction. The Parkinson's Disease Foundation estimates that there are approximately one million people living with Parkinson's disease in the United States and seven to 10 million PD patients worldwide. The most commonly prescribed treatments for Parkinson's disease are levodopa-based therapies. In the body, levodopa is converted to dopamine to replace the dopamine loss caused by the disease. As dopamine neurons in the brain are lost the therapeutic efficacy of levodopa attenuates, and increased use is associated with a side effect of dyskinesias. These are involuntary, uncontrollable and often exaggerated and jerky movements. They are distinct from the static, rhythmic tremor as a symptom of Parkinson's disease. Levodopa-induced dyskinesia can be severely disabling, rendering patients unable to perform routine daily tasks.

About Amarantus BioScience Holdings, Inc.

Amarantus BioScience Holdings (AMBS) is a biotechnology company focused on developing diagnostics in neurology, and therapeutic products with the potential for orphan drug designation in the areas of neurology, psychiatry, ophthalmology and regenerative medicine. AMBS has licensed Eltoprazine, a Phase 2b ready small molecule indicated for Parkinson's disease Levodopa-induced dyskinesia and adult ADHD. AMBS has an exclusive worldwide license to the Lymphocyte Proliferation test, (LymPro Test^®), which was developed by Prof. Thomas Arendt, Ph.D., from the University of Leipzig, for Alzheimer's disease and owns the intellectual property rights to a therapeutic protein known as mesencephalic-astrocyte-derived neurotrophic factor ("MANF") and is developing MANF-based products as treatments for brain and ophthalmic disorders. AMBS also owns intellectual property for the diagnosis of Parkinson's disease (NuroPro) and the discovery of neurotrophic factors (PhenoGuard^™).

In November 2014, AMBS entered into an exclusive option agreement with Lonza Walkersville, Inc., a subsidiary of Lonza Group Ltd., to acquire Cutanogen Corporation, a subsidiary of Lonza Walkersville, to develop Engineered Skin Substitute (ESS-W), an autologous skin replacement product for the treatment of Stage 3 and Stage 4 intractable severe burns.

On January 12, 2015, AMBS announced the acquisition of DioGenix, Inc., a specialized neuro-diagnostics company, and owns the rights to MSPrecise^®, a proprietary next-generation DNA sequencing (NGS) assay for the identification of patients with relapsing-remitting multiple sclerosis (RRMS) at first clinical presentation. On January 15, 2015, AMBS executed a one-year exclusive option agreement with Georgetown University to enter into a license for the patent rights related to certain blood based biomarkers for memory loss and Alzheimer's disease jointly owned by Georgetown University and University of Rochester. For further information please visit www.Amarantus.com, or connect with the Company on Facebook, LinkedIn, Twitter and Google+.

About Our Collaboration Partners

Karolinska Institutet is one of the world's leading medical universities. Its vision is to significantly contribute to the improvement of human health. Karolinska Institutet accounts for over 40 percent of the medical academic research conducted in Sweden and offers the country's broadest range of education in medicine and health sciences. The Nobel Assembly at Karolinska Institutet selects the Nobel laureates in Physiology or Medicine.

The Faculty of Medicine at Lund University works to understand, explain and improve human health. As a part of Lund University we create unique interdisciplinary collaborations for scientific breakthroughs and innovations. Lund University was founded in 1666 and is consistently ranked among the world's top 100 universities.

Forward-Looking Statements

Certain statements, other than purely historical information, including estimates, projections, statements relating to our business plans, objectives, and expected operating results, and the assumptions upon which those statements are based, are forward-looking statements. These forward-looking statements generally are identified by the words "believes," "project," "expects," "anticipates," "estimates," "intends," "strategy," "plan," "may," "will," "would," "will be," "will continue," "will likely result," and similar expressions. Forward-looking statements are based on current expectations and assumptions that are subject to risks and uncertainties which may cause actual results to differ materially from the forward-looking statements. Our ability to predict results or the actual effect of future plans or strategies is inherently uncertain. Factors which could have a material adverse effect on our operations and future prospects on a consolidated basis include, but are not limited to: changes in economic conditions, legislative/regulatory changes, availability of capital, interest rates, competition, and generally accepted accounting principles. These risks and uncertainties should also be considered in evaluating forward-looking statements and undue reliance should not be placed on such statements.

CONTACT: Investor and Media Contact: Jenene Thomas Jenene Thomas Communications, LLC Investor Relations and Corporate Communications Advisor T: (US) 908.938.1475 E: jenene@jenenethomascommunications.com

Source:Amarantus BioScience Holdings, Inc.

The Stigma of Parkinson’s Disease

FoxFeed Blog

Posted by  Rachel Dolhun, MD, February 09, 2015

The hallmark signs of Parkinson’s disease — tremor, stiffness, slowness and/or walking problems — are fairly obvious to the outside observer. Less apparent non-motor symptoms, such as depression, anxiety and apathy, are also often present.

Both aspects of Parkinson’s — visible and invisible — can be misinterpreted, causing a stigma sometimes associated with neurological disease.  Slowness of movement or speech may be perceived as intellectual disability, imbalance as intoxication, masked facial expression as an unfriendly demeanor, and tremor as nervousness. Internalizing these judgments or trying to hide the disease to avoid discrimination only make symptoms worse.

Nancy Mulhearn, a person living with Parkinson’s disease, recently shared her approach to challenging social stigma with Neurology Now:

                     “I recommend surrounding yourself with a network of people dealing with the same
                      problem… I didn't want to be pitied or stared at, and I didn't want the world to change
                      for me and my condition,” she explains.

By openly sharing their personal experiences with Parkinson’s, people like Nancy are helping to educate others. One person and one story at a time, we can work to gradually dissolve the social stigma associated with neurological diseases like Parkinson’s..

Turn Staring Into Caring: The stigma of a neurologic disorder can be stressful—and can make symptoms worse. Patients and doctors teach us how to turn negative reactions into positive encounters.

Neurology Now

February/March 2015

 

Volume 11(1)

 

p 34–38

Stephens, Stephanie

Illustrations by Brian Stauffer

Back to top

When Stephanie Schroeder rolls and blinks her eyes, shrugs her shoulders, or opens her mouth and stretches her tongue, people sometimes stare, and she feels it.

“People may think my contacts are bothering me or that I have a neck ache,” says 51-year-old Schroeder, of Brooklyn, NY. “When I first moved to New York, kids on the subway would laugh and point. Riding the subway definitely gave me a pretty thick skin.”

That thick skin helps protect Schroeder from the unwelcome reactions of strangers to the visible symptoms of Tourette syndrome, with which she was diagnosed 24 years ago. She's happy to “tell all” to those who ask about her tics and is often amused by the responses. “Once I told someone at work and he just chuckled uncomfortably, ‘That's cool. I don't know anybody else with Tourette's.’”

Of course, the discomfort others feel toward her tics hasn't always been so benign. In fact, she thinks she has probably failed in job interviews because of her condition. “I just knew they wouldn't hire me, even though I have no proof of that. Maybe they thought, ‘Why is this crazy lady moving around so much?’” (For more information about workplace discrimination, see “Work Disclosure: When Is It Safe?” on page 38.)

Tourette's is just one of many neurologic conditions with visible symptoms that can make strangers uncomfortable, afraid, or react inappropriately. And dealing with those negative reactions can be upsetting for the recipients—and can even exacerbate certain symptoms.

STIGMA CAUSES STRESS

“If you come see me as an adult patient and you have frequent and noticeable motor and/or vocal tics, I know you've probably been the victim of a fair amount of stigma,” says James Frederick Leckman, MD, a professor of pediatrics and psychiatry and the Neison Harris Professor in the Child Study Center at Yale School of Medicine. Being repeatedly singled out and mimicked can even cause a form of post-traumatic stress disorder, or PTSD, he says. He's known patients to report flashbacks and nightmares. Some avoid places where they experienced painful teasing, while others remain wary and watchful and have trouble concentrating.

Sometimes even well-meaning people can contribute to the stigma, says Dr. Leckman. A teacher who doesn't understand or recognize the symptoms of Tourette's, for instance, may ask a child to “stop” his or her “bad” behavior. If the teacher subsequently disciplines that child, the teacher may be unknowingly encouraging other kids in class to mistreat that student, causing more stress and potentially making the tics worse.

USING FAME TO COUNTER SHAME

Parkinson's disease is another neurologic disorder with outward symptoms that are frequently misinterpreted. A tremor can be misread as anxiety or nervousness, an unsteady gait can mistakenly convey intoxication, and slurred speech may falsely suggest intellectual disability, all of which can make social interaction difficult, says Rachel Dolhun, MD, a medical communications specialist for the Michael J. Fox Foundation for Parkinson's Research. In some cases, the disease can cause a loss of facial expression, making it difficult for Parkinson's patients to convey their emotions, which others may interpret as unfriendly or standoffish, she adds.

The stigma of the disease may have been why Michael J. Fox, the Back to the Future actor and one of the more famous faces of the disease, waited seven years before disclosing his condition. Since going public and christening his foundation 14 years ago, Fox has earned international respect for his efforts to find a cure and eradicate stigma by being open and honest and by raising public awareness. As he told a New York Times op-ed columnist, “many Parkinson's sufferers feel shame,” and he has worked to help take the shame out of the disease.

n his television comedy, The Michael J. Fox Show, which aired on NBC between September 2013 and January 2014, his character, Mike Henry, had Parkinson's. Like the actor, Henry openly acknowledged his condition, as well as the unwanted attention it brought, often with humor.

During an appearance last November on NBC's Today show with co-host Willie Geist, whose father, CBS Morning correspondent Bill Geist, has the disease, Fox acknowledged the shame that accompanies having any illness, including Parkinson's. But he said he's proud to be the public face of the disease. “Since I made my diagnosis known, it's been a tremendous opportunity and a tremendous privilege,” he said.

SEEKING AND GIVING SUPPORT

“I recommend surrounding yourself with a network of people dealing with the same problem,” says Nancy Mulhearn of Asbury, NJ, who was diagnosed with Parkinson's in 2006 at age 44. That's what she did after years of denying the disease and hiding her symptoms. “I didn't want to be pitied or stared at, and I didn't want the world to change for me and my condition,” she explains.

Reach Out to Reduce Stigma

Limited communication and interaction between patients with neurologic disorders and the general public can increase the misunderstandings that lead to stigma, says Patrick Corrigan, PsyD, principal investigator at the National Consortium on Stigma and Empowerment and distinguished professor of psychology at the Illinois Institute of Technology.

Dr. Corrigan advocates for more “face time” between the two communities, advising people to “meet and get to know that person with the disorder. Sitting at church or working alongside someone can disarm prejudice and reframe misconceptions, while combining different points of view,” he says.

* Get Connected. Health care providers can help, too, says Deepa Rao, PhD, an associate professor in the departments of global health and psychiatry and behavioral sciences at the University of Washington. For example, they can connect patients with similar conditions who can support one another. That's what Dr. Rao sought out for her daughter, who has a medical condition; she asked her daughter's physician for the names of other families who were dealing with the same challenges.The Health Insurance Portability and Accountability Act (HIPAA), which governs patients' privacy rights, prevents physicians from sharing names, Dr. Rao notes. But patients can sign a privacy release form to give their doctor permission to share their names. “This helps us feel like we're not alone,” Dr. Rao says. “We all learn coping mechanisms by modeling each other's behaviors.”

* Be Kind to Yourself.“Self-stigma is an egregious impact of stigma in general, a diminished sense of self-esteem leading to a ‘Why try?’ attitude in many people,” says Dr. Corrigan. He thinks that the focus on “patient-centered outcomes” in the Affordable Care Act presents an opportunity for the health care profession to empower patients with neurologic disorders. “We can help them better determine their health care options and personal goals and learn to make decisions for themselves. All of that reduces self-stigma.”

* Dare to Share. Talking openly about symptoms can take a bite out of stigma and its effects. That's why Stephanie Schroeder does it. “My tics are part of who I am and don't really bother me unless I'm unduly stressed,” she says. “What does bother me is the amount of negative energy other people spend trying to shame me and others with Tourette's. It says more about them than about me or the disorder.”

When she could no longer disguise her symptoms, Mulhearn attended a Fox Foundation conference to learn more—and that changed her life. She says she was motivated and inspired to get involved by those she met at the conference. Now, at age 53, she's helped raise more than $100,000 for the foundation by organizing gala events. She's also a member of Team Fox, the grassroots community fundraising program, for which she mentors people who have been diagnosed with Parkinson's.

I've experienced every emotion: depression, denial, and more,” says Mulhearn. “I know what they are feeling and I can help.”

As for strangers' curiosity, she addresses it head on. “If I'm fumbling for change, I say, ‘I have Parkinson's disease,’” she explains. “I could go hide, but if other people see I'm OK with this, they're usually OK, too.”

COUNTERING THE CULTURE

Sometimes, people are frightened by neurologic illness simply because what they've heard about the condition and its symptoms is far worse than the reality. That's especially true with epilepsy, says Wendy Miller, PhD, RN, CCRN, an assistant professor at the Indiana University School of Nursing and a member of the professional advisory board for the Epilepsy Foundation.

“Movies and media can totally misrepresent epilepsy,” says Dr. Miller. “It's important to explain that, yes, you may have seizures, but that doesn't mean you'll soon be falling on the ground. You may just stare into space for a while.”

In 2013, Jerry Krill, the head coach of the University of Minnesota football team, noticed that his epileptic seizures were becoming more frequent. When he had one on the field during a game, some people called for his resignation.

The public outcry had a positive outcome. It forced Krill to reassess his workaholic habits and it prompted moral support from the university and the football team. Today, Krill eats healthier and gets enough sleep, and hasn't had a seizure in more than a year. And he has scored high points for helping to eradicate stigma.

The Epilepsy Foundation urges people with epilepsy to explain how their seizures look to those with whom they are in daily contact. “Tell them this is not a mental condition and it's not contagious,” Dr. Miller advises.

FIGHTING SKEPTICISM

A lifelong migraineur (a person who experiences migraines), Anjan Chatterjee, MD, MPH, MBA, is intimately familiar with the debilitating pain, nausea, vomiting, and sensitivity to light caused by migraine headaches, making him particularly empathetic to his migraine patients. He recalls the lack of sensitivity he encountered in medical school and during his residency, when studying for tests and working unreasonably long hours exacerbated his migraines and caused him to retreat for long periods of time.

That didn't go unnoticed, he says. “Even the most caring neurologist might say, ‘It's just a headache, now, isn't it?’ You may not be criticized if you had Parkinson's, but others may think a headache is just an excuse. People with migraine face that stigma time and time again and may worry about losing their jobs.”

That skepticism doesn't happen only at work, Dr. Chatterjee adds. “Patients have separated and divorced because their partners just don't believe them.”

When consulting with headache patients, Dr. Chatterjee, a member of the American Academy of Neurology and a Fellow of the American Headache Society, invites the entire family to learn more about what their loved one is experiencing. “I think 99 percent of the time, when you clearly explain this condition, a person's attitude changes from one of cynicism to extreme support,” he says. “Patients are the best people, even more so than health care professionals, to advise other patients about how to deal with stigma.”

BATTLING BIAS

Obvious symptoms often invite stares and whispers, but hidden symptoms such as some cognitive deficits associated with brain injury can be judged even more harshly, says Donna Langenbahn, PhD, a clinical associate professor at Rusk Rehabilitation at NYU Langone Medical Center. People with brain injuries—whether from car accidents, sports injuries, falls, or assaults—may be deemed “stupid or inept without an understanding of the underlying cause,” she says.

That bias may render them “less of a person” in the eyes of others, says Dr. Langenbahn, who urges people to let go of their biases and learn more about brain injury and how it may affect aspects of life such as work, school, play, leisure, and intimacy. “That allows the person to maintain an active role in society and, ultimately, a sense of dignity.”

KNOW THE BASICS:

* Parkinson's Disease: The Basics—bit.ly/basics-PD

* Epilepsy: The Basics—bit.ly/Epilepsy-Basics

* Migraine: The Basics—bit.ly/Migraine-Basics

* Traumatic Brain Injury: The Basics—bit.ly/TBI-Basics

* Tourette Syndrome: AAN resources for patients —bit.ly/AAN-Tourette

Many people with a neurologic disorder who want and need to work are dogged by the question: to tell or not to tell? Indeed, there's a lot at stake, says Patrick Corrigan, PsyD, principal investigator at the National Consortium on Stigma and Empowerment and distinguished professor of psychology at the Illinois Institute of Technology.

“People who can hide a neurological disorder must decide carefully whether they want to [reveal their condition],” he says. “‘Coming out’ or disclosing can be a huge decision, especially if the condition is misunderstood. For example, just because I see you having symptoms, doesn't mean I understand what the disorder is or does. And just because the medical community understands, doesn't mean the public does.”

The employment arena is rife with discrimination, says Dr. Corrigan, who has published studies on the topic. “People with neurological conditions are less likely to be hired and less likely to be provided reasonable accommodations guaranteed by the Americans with Disabilities Act of 1990.”

The law prohibits discrimination and ensures equal opportunity for persons with disabilities in employment, state and local government services, public accommodations, commercial facilities, and transportation, he says. “If you're in a wheelchair, your employer is legally bound to provide accommodations for you, like revamping your workplace for accessibility. The same is legally true for people with neurologic disorders—those accommodations might include a job coach or a social worker.”

“Remember that you can't be fired for having a disability,” says Wendy Miller, PhD, RN, an assistant professor at the Indiana University School of Nursing and a member of the professional advisory board for the Epilepsy Foundation. “Not everyone you work with needs to know, but disclosing to those in close proximity may be a good idea to the degree that you're comfortable. The worst thing could be that no one knows you have the condition, and they don't know what to do when you need them.”

WEB EXTRAS:

* For how to combat stigma or to listen to a podcast about stigma and epilepsy, go to bit.ly/NN-stigma

http://patients.aan.com/resources/neurologynow/index.cfm?event=home.showArticle&id=ovid%2Ecom%3A%2Fbib%2Fovftdb%2F01222928-201511010-00017