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I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's
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Friday, April 22, 2016

Parkinson’s Physical and Cognitive Symptoms May Be Based in Same Brain Region, Study Suggests

  • APRIL 22, 2016
University of California, San Diego, study shows that the same brain system involved in a sudden stop in physical movement also interrupts cognitive processes. The findings hold implications for Parkinson’s disease, where cognitive impairment is a major symptom.
The study, Surprise disrupts cognition via a fronto-basal ganglia suppressive mechanism, focused on a deep brain structure known as the subthalamic nucleus (STN), which is part of the basal ganglia, a group of structures involved in the coordination of movement — and the very structure targeted in deep brain stimulation, a therapeutic technique used in Parkinson’s.
Researchers at UC San Diego have previously shown that this region is active when a sudden interruption of movement is required. In Parkinson’s, an over-activation of the stopping system might cause the slowed-down movement and facial expressions characteristic of the disease. If the new findings are confirmed in future studies, STN will also be shown to contribute to disturbed cognitive processes.
Published in the journal Nature Communicationsthe study analyzed signals from the STN region in 20 healthy volunteers using scalp electrodes, and in seven Parkinson’s patients with electrode implants in the STN brain region.
All participants received a working memory task, consisting of remembering a string of letters. Before they were asked to recall the letters, a simple, single-frequency tone was played. But in some tests, the tone was replaced by a birdsong — an unexpected event. Researchers noted that this surprise activated the STN in the same way as stopping body movement. The more active the region, the worse the participants performed on the memory test. Recordings from the scalp and deep brain electrodes showed similar results.
“For now, we’ve shown that unexpected, or surprising, events recruit the same brain system we use to actively stop our actions, which, in turn, appears to influence the degree to which such surprising events affect our ongoing trains of thought,” Jan Wessel, the study’s first author and now an assistant professor of psychology and neurology at the University of Iowa, said in a press release.
“An unexpected event appears to clear out what you were thinking,” said Adam Aron, a professor of psychology at UC San Diego. “The radically new idea is that just as the brain’s stopping mechanism is involved in stopping what we’re doing with our bodies, it might also be responsible for interrupting and flushing out our thoughts.”

Scientists at the MDI Biological Laboratory Are Unlocking the Mechanisms of Parkinson’s Disease

Scientists at the MDI Biological Laboratory Are Unlocking the Mechanisms of Parkinson’s Disease

Designation of April as Parkinson’s Awareness Month Highlights Need for Cure

April 21, 2016
BAR HARBOR, MAINE – Scientists at the MDI Biological Laboratory are identifying the basic mechanisms behind Parkinson’s disease, a degenerative neurological disease affecting millions of people worldwide. The research could some day  to treatments for a disabling condition for which medicine now has nothing to offer other than symptomatic relief.
The designation of April as Parkinson’s Awareness Month has called attention to the need for treatments for this disease, a progressive disorder of the nervous system that causes tremors, stiffness, slowed movement and  balance and coordination. The disease affects nearly 1 million people in the United States alone and is age-related: the average age of onset is 60 and the incidence rises sharply with age.
Although many scientists study Parkinson’s in the context of its hereditary basis, most cases are sporadic, meaning they are not associated with a disease-causing mutation in a single gene. MDI Biological Laboratory assistant professor Aric Rogers, Ph.D., and his team are investigating ways of enhancing basic mechanisms to keep cells healthy and resistant to the conditions that can lead to Parkinson’s.
“Rather than trying to fix genes that may or may not contribute to Parkinson’s disease on a case-by-case basis, we’re studying genes with the potential to strengthen cellular systems, including one gene that we consider to be a master regulator of protein synthesis in the cell,” he explained.
The MDI Biological Laboratory, in Bar Harbor, Maine, is an independent, nonprofit biomedical research institution focused on increasing healthy lifespan and harnessing the natural ability to repair and regenerate tissues damaged by injury or disease. The institution develops solutions to complex human and environmental health problems through research, education and ventures that transform discoveries into cures.
Rogers and other scientists working in the institution’s Kathryn W. Davis Center for Regenerative Medicine study tissue repair, regeneration and aging using a diverse range of model organisms.
“The Parkinson’s Awareness Month designation calls attention to the fact that there is no cure for this disease, which is becoming increasingly prevalent as the world’s population ages,” said Kevin Strange, Ph.D., the MDI Biological Laboratory’s president. “Aric Rogers’ important work reflects our mission of developing treatments that address the underlying causes — rather than the symptoms — of age-related disorders.”
All animals need to manufacture new and different proteins to perform various functions. When Rogers’ team “turned down” the activity of the protein synthesis regulator gene in the tiny roundworm, C. elegans, they were able to reduce the toxicity of malformed proteins associated with Parkinson’s disease. They were also able to redirect remaining protein synthesis capability toward maintaining cellular health.
“By lowering the activity of a specific gene, we were able to ‘tighten the belt’ on protein synthesis and shift remaining production toward proteins whose job it is to keep cells healthy,” said Rogers. “The effect was dramatic — by targeting a single gene, we saw an 80 percent decrease in Parkinson’s-associated toxicity. This suggests that Parkinson’s is linked to an inability to properly regulate proteins in the cell.”
The understanding of molecular pathways gained through Rogers’ research raises the prospect that drugs can be developed for use in humans to turn down the production of proteins that can become toxic, such as alpha-synuclein, which has been linked with Parkinson’s disease, or beta-amyloid, which is associated with Alzheimer’s disease – or even the unrestrained cell growth associated with cancer, Rogers said.
Rogers was inspired to explore the role of protein synthesis in Parkinson’s by his work on the effect of dietary restriction on aging. Dietary restriction lowers protein synthesis and has been known since the 1930s to extend lifespan in rodents. Since then, it has been shown to increase lifespan and ameliorate the effects of age-related chronic diseases in diverse species from yeast to primates.
Rogers is now applying the techniques employed in his research on dietary restriction to neurodegenerative disorders. Because the protein synthesis regulator gene that Rogers’ team is studying becomes less active when food is scarce, he believes that by turning down the activity of this gene, his team may be tapping into an adaptive survival response to improve human health and affect disease outcomes.
His laboratory uses the tiny roundworm, C. elegans, as a model because it shares many of its genes with humans and because its three-week lifecycle allows scientists to quickly test how genes affect disease and longevity.
The MDI Biological Laboratory, located in Bar Harbor, Maine, is an independent, non-profit biomedical research institution focused on increasing healthy lifespan and increasing our natural ability to repair and regenerate tissues damaged by injury or disease. The institution develops solutions to complex human health problems through research, education and ventures that transform discoveries into cures. For more information, please visit

Thursday, April 21, 2016

Penn Medicine Awarded Fellowship to Train Next Generation of Parkinson’s Specialists

Michael J. Fox Foundation & Edmond J. Safra Foundation support training to increase movement disorder professionals


The University of Pennsylvania Parkinson’s Disease and Movement Disorders Center has been chosen to host the 2017-2019 Edmond J. Safra Fellowship in Movement Disorders by The Michael J. Fox Foundation, in collaboration with its longtime supporter and partner the Edmond J. Safra Foundation. The Safra Fellowship program supports training to expand the number of movement disorder specialists treating and researching Parkinson’s disease.

Penn is one of five academic medical centers in the United States (and one in Germany) to host the second class of the Safra Fellowship in Movement Disorders. The five US centers will now identify a fellow to begin two years of training in July 2017. The University of Tübingen in Germany has identified a fellow to begin later in 2016. The other four US awardees are Icahn School of Medicine at Mount Sinai in New York; University of California San Francisco; Rush University in Chicago; and the University of Rochester in Rochester, New York.

Under the direction of Penn’s fellowship director Nabila Dahodwala, MD, MS, an assistant professor of Neurology at the Perelman School of Medicine at the University of Pennsylvania, and associate fellowship director, Lama Chahine, MD, the fellowship will feature a two-year personalized training program tailored to the specific needs of the fellow. Foundational features will include a general movement disorders clinical experience, including extensive hands-on experience with chemodenervation (the use of Botulinum Toxin to treat various forms of neurological conditions) and deep brain stimulation programming (via an implanted device similar to a pacemaker). Several specialized rotations in neurogenetics, dementia, neuro-ophthalmology, neuropsychiatry, and ataxia (lack of voluntary coordination of muscle movements, including walking abnormality) are also available.
The to-be-identified fellow will also participate in two multi-disciplinary clinics that focus on atypical Parkinsonism and pre-surgical evaluation for Parkinson patients. In addition, he/she will take part in a continuity outpatient clinic by evaluating new movement disorders patients and following them for two years to learn how to independently diagnose and manage movement disorders under the supervision of movement disorder faculty.

“This program trains knowledgeable specialists who provide day-to-day care to people with Parkinson’s and conduct research to speed the development of new treatments,” said Todd Sherer, PhD, CEO of The Michael J. Fox Foundation. “There is a pressing need for both sides of service as our population grows and more people age into risk of Parkinson’s disease.”

Research opportunities for the new fellow at Penn will include bench-based research on alpha-synuclein pathology (alpha-synuclein is a protein that experts know plays a role in the development of Parkinson's disease), Parkinson’s disease biomarker discovery, experimental neurotherapeutic clinical trials and health outcomes research. With the mentorship of a large and diverse faculty including Dr.’s Matthew Stern, Virginia Lee, John Trojanowski, Murray Grossman and Daniel Weintraub, among many others, the fellow will have the opportunity to develop an independent research program. 
The Safra Fellowship is named for Edmond J. Safra, widely viewed as one of the most accomplished bankers of the 20th century, having established a business that spanned more than thirty countries across the globe. Recognized worldwide for his philanthropy, Mr. Safra was named Commandeur de l’Ordre des Arts et des Lettres and Chevalier de la Légion d’Honneur by the French government; Commandeur de l’Ordre de Mérite by the Grand Duke of Luxembourg; and Commandeur de l’Ordre de Rio Branco by the government of Brazil. He died in 1999.

Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $5.3 billion enterprise.

The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 18 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $373 million awarded in the 2015 fiscal year.
The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center -- which are recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report -- Chester County Hospital; Lancaster General Health; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Chestnut Hill Hospital and Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine.
Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2015, Penn Medicine provided $253.3 million to benefit our community.

A Baby Boomer With Parkinson's Reports Back From Front Lines Of Aging

April 21, 2016

Michael Kinsley

Journalist Michael Kinsley — the founder of Slate and former editor of Harper's and The New Republic — says he's a "scout for his generation." Kinsley was diagnosed with Parkinson's Disease when he was in his 40s. Now in his 60s, he writes that he had the opportunity to experience old age before the rest of his fellow baby boomers.
"There are far worse medical conditions than Parkinson's, and there are far worse cases of Parkinson's than mine," he writes, "But what I have, at the level I have it, is an interesting foretaste of our shared future."
Kinsley reports back on what he's learned in a new book called Old Age: A Beginner's Guide.
I think many people have seen [old age] in the course of taking care of their parents," he tells NPR's Robert Siegel. "But I don't think it's clicked that: Wait a minute, we're now our parents. We have to do something to make it better."

Interview Highlights

On Parkinson's having cognitive effects as well as physical effects
I was unhappily surprised to discover it does. People thought of it as a movement [disorder] — you go to movement clinics to treat it — but in fact, in the past 20 years actually since I was diagnosed, they've discovered a lot of cognitive effects. It's not like Alzheimer's where the cognitive decline is absolutely certain, but it's much more common than people previously realized.
On whether people treated him differently once they learned he had Parkinson's
Not totally differently but certainly differently. ... When I came out as a "Parkinsonian," as they call it, I was treated differently. Not that anyone's been mean to me — in fact they're excruciatingly nice — they want to cut up my meat for me at a dinner party ... A very nice woman said, "Can I cut up your meat for you?" and that can be excruciating even though it's totally well-meant.
On continuing to write columns for Vanity Fair, and whether it takes longer than it used to

CRISPR Aids Identification of Sporadic Parkinson’s Mutation in GWAS

                                                           Jonathan Bailey, NHGRI

April 21, 2016
The overwhelming majority of Parkinson’s disease (PD) and Alzheimer’s disease cases that occur are sporadic—caused by a complex mix of environmental and shared genetic factors. These types of interactions are notoriously difficult for scientists to study, which is why most research has focused on familial cases that have much clearer genetic origins.
Now, investigators at the Whitehead Institute have determined how a noncoding mutation identified in genome-wide association studies (GWAS) can contribute to sporadic PD. The researchers are hopeful that their novel approach will be helpful in analyzing future GWAS results for other sporadic diseases with genetic causes, such as Alzheimer’s, multiple sclerosis, diabetes, and cancer.   
Researchers discover how a noncoding mutation identified in genome-wide association studies can contribute to sporadic Parkinson's disease.[NIH]"
This is really the first time we've gone from risk variants highlighted by GWAS to a mechanistic and molecular understanding—right down to the nucleotide—of how a mutation can contribute to the risk of developing disease," explained senior study author Rudolf Jaenisch, M.D., Whitehead Institute founding member and professor of biology at MIT.
Scientists often view GWAS as a treasure trove of genomic information marking the general locations of mutations that could be risk factors for a given condition. Yet, GWAS do not reveal the precise locations of potentially pathogenic mutations, nor do they indicate how a particular locus on a genomic map contributes, if at all, to a disease. For instance, in sporadic PD, multiple GWAS have pointed to the α-synuclein gene (SNCA) as one of the strongest risk loci in patients' genomes. However, the GWAS contain little information regarding the mechanism of how this gene is dysregulated in sporadic PD patients.
To determine if distant gene regulatory elements on the same chromosome carrying SNCA affected cellular levels of α-synuclein, the Whitehead team investigated two GWAS-flagged risk variants located in a putative SNCA enhancer.
The researchers then used the CRISPR/Cas9 genome editing system to modify the mutations into isogenic human pluripotent stem cells. By altering the genetic variant on only one chromosome, the other chromosome remains unchanged and acts as an internal control. This method allows the scientists to measure very subtle effects with very high confidence while eliminating the effect of any genetic or epigenetic modifications and cell culture related variations that could occur during the experiment.
“Here we describe a novel strategy to functionally dissect the cis-acting effect of genetic risk variants in regulatory elements on gene expression by combining genome-wide epigenetic information with clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 genome editing in human pluripotent stem cells,” the authors wrote. “By generating a genetically precisely controlled experimental system, we identify a common Parkinson’s disease associated risk variant in a non-coding distal enhancer element that regulates the expression of α-synuclein (SNCA), a key gene implicated in the pathogenesis of Parkinson’s disease.”
The findings from this study were published recently in Nature in an article entitled "Parkinson-Associated Risk Variant in Distal Enhancer of α-Synuclein Modulates Target Gene Expression."
"Our method addresses an essential shortcoming of GWAS—using the correlations produced by GWAS, you cannot distinguish the effect between two variants that are very close together in the genome," noted lead study author Frank Soldner, M.D., senior research scientist in Dr. Jaenisch’s laboratory. "Such physical proximity means that they will always co-segregate during inheritance, which is why we had to do what we did—modify and analyze each variant independently while keeping the rest of the genome completely constant."
Once the Whitehead team differentiated the stem cells into neurons, they took careful note of the changes in SNCA expression. While one of the mutations had no effect, the other, which switches one nucleotide from an A to a G, slightly but significantly, boosts SNCA production. When compared to the enhanced SCNA production in the familial form of the disease, the modest effect created by the A-to-G mutation would be sufficient over a lifetime to increase the risk of PD, the researcher postulated.
To see how the mutation affects α-synuclein production, the researchers identified two transcription factors that bind to the enhancer carrying this mutation. When the enhancer was not mutated, the transcription factors bind to it normally and suppress SNCA production. If the enhancer had the G mutation, the transcription factors were unable to bind to the enhancer, and SNCA production is activated.
The research team was excited by their findings and looking to apply their novel technique used to pinpoint additional pathogenic genes for sporadic PD and sift through the GWAS hits for other diseases.

Parkinson’s disease patient from Ipswich tells his emotional story as new research reveals 42% of people in the region have felt the need to hide their diagnosi

21 April 2016

James Scott speaks about his experience with Parkinson's disease
An Ipswich man who was diagnosed with Parkinson’s disease four years ago has spoken about why he kept his symptoms hidden from his family and how the condition has impacted his life.

New research released by Parkinson’s UK to mark Parkinson’s Awareness Week shows that 42% of people in the East of England have felt the need to lie about having the disease due to fear or embarrassment. 
James Scott was working as a high-earning English tutor in Moscow where he lived with his partner and young daughter when he first realised something was wrong.
Mr Scott started to get stiffness in his left arm and hand, a throbbing in his head and he developed a chronic stammer.
“I initially tried to hide my symptoms. I would pretend everything was normal, and tried to carry on as if nothing was happening,” he said.

James Scott and his father Ray, who also recently been dignosed with Parkinson's disease.
“My partner knew something was up. For around two years I tried to pretend nothing happened. After considerable questioning, she forced me to seek medical advice. 
“I paid to see the best medical professionals in Moscow. I was told bluntly by a neurologist that I had Parkinson’s. There was no support and no help offered. I was told I had Parkinson’s and had to live with it.
“In the time I knew something was wrong, but had not been diagnosed, I spent many evenings crying and drinking and trying not to feel sorry for myself. I suffered alone, and would not open up about it. I guess I was being typically English, trying to have a stiff upper lip and dealing with it in my own way.”
Mr Scott, who grew up in Ipswich and attended St Alban’s Catholic High School, was diagnosed with Parkinson’s disease at the age of 48 – 12 years younger than the average age of onset.
Teaching became more and more difficult as Mr Scott’s students noticed that he was struggling to speak.
Last July he returned back to his family home in Goring Road, Ipswich, to live with his 87-year-old father Ray Scott, who was also diagnosed with Parkinson’s about three months ago. 
“I could not afford to live in Russia,” Mr Scott added. “I had to frequently return to England because of my Parkinson’s, alongside paying for speech therapy and spending large amounts on medication and costly brain scans. 
“I felt I was slowing down my family. It was heart-breaking telling my family I was leaving Moscow.”
The now 51-year-old has regular contact with his teenage daughter Alex, who is still living and studying in Russia, but he said he struggled with the distance between them. 
Mr Scott now wears a wristband that says: ‘I have Parkinson’s please give me time’, so people understand why he acts and speaks slower.
“I get the impression that people look at me and think, ‘he’s a bit weird, there’s something wrong with him’,” he said. “People in shops immediately and instinctively realise this chap is not all there, a sandwich short of a picnic. 
“It’s quite upsetting but I just want to reassure them that I may come across like a zombie but I’m really just a regular guy underneath that.
“I’ve got a good sense of humour but it’s difficult for it to come out, especially witty comments – I can’t get them out in the time and by the time I say it the moment has gone. 
“I certainly feel much more comfortable in the presence of other people with Parkinson’s.”
Around six months ago, Mr Scott teamed up with charity Parkinson’s UK to set up a support group in Suffolk for working-age people with the condition. 
It is called 24 Hour Parky People and the group meets every three weeks at Martlesham Black Tiles pub. 
“Maybe it’s cold comfort but knowing that other people are experiencing the same symptoms can help,” Mr Scott said. “The best way of describing Parkinson’s is you are just 
not with it, you are just not switched on.
“It’s sometimes like I’m looking down on myself, like a feeling of being dizzy but not being dizzy. 
“Certainly on the one hand since I’ve been back in Ipswich life has been a much slower pace, less hectic and demanding, and my dad has been very good to me, but if I’m honest there has been a slight deterioration.”
For the past year Mr Scott has been a member of Ipswich JAFFA Running Club and he said running with others helped him cope with his symptoms.
“The thing I like about running is you can quite easily chat to people – there’s a sense of belonging when wearing the club shirt,” he said.
“Also when I’m running people tend not to notice I have a bit of speech impediment because I just come across as someone who is struggling with running.”
For advice or information about Parkinson’s disease, visit: or call the free helpline on 0808 800 0303.

Exercise may slow symptoms of Parkinson’s disease

Graciela Gutierrez713-798-4710Houston, TX

he benefits of exercise are numerous, even for those diagnosed with a neurodegenerative disorder such as Parkinson’s disease. Experts at Baylor College of Medicine’s Parkinson’s Disease and Movement Disorder Clinic (PDMDC) say that for some, regular exercise could even slow the progression of the disease. 
Parkinson's disease is a disorder of the nervous system that affects movement. It develops gradually and may progress to cause difficulties with mobility and balance. The most common symptoms are tremor and/or stiffness and for some, these symptoms can become disabling without the help of medications.
“A person with Parkinson’s disease becomes less able to regulate their body and limb movements as time goes on. Exercise helps by building stamina, strength and maintaining a range of motion,” said Dr. Joseph Jankovic, professor of neurology at Baylor and Director of the PDCMDC. “Exercise has been shown to help improve flexibility, walking, grip strength and coordination.”
So what kind of exercises are best? Jankovic says that depends on what stage of Parkinson’s disease a person is living with. It is important to speak to your doctor to determine what is right for your individual health and abilities, however the key is consistency.
Not only has exercise been shown to support physical health but also brain health. In Parkinson’s disease, certain neurons, including those that produce dopamine, stop functioning and the production of dopamine decreases.
Some studies have shown that when exercise is introduced, the brain begins to use dopamine more efficiently. There is also research that supports the idea that neuroplasticity (the brain’s ability to adapt or compensate to changes in function) is supported by exercise, helping the brain to maintain and strengthen neural connections. It is believed that this plays a role in slowing the progression of the disease.
“While there is no cure for Parkinson’s disease, there are medications available and when coupled with lifestyle changes, such as vigorous exercise program, most Parkinson’s patients can continue to enjoy meaningful quality of life and well-being,” said Jankovic.

Greenville couple help Strike Out Parkinson's

Ken and Susan Smith
Greenville, SC

April 21, 2016
Ken Smith was the fixer-upper in his household, the one always tinkering with something, his wife said.
But one day, the hands that fixed things began having difficulty with simply writing a check.
That prompted a visit to the family doctor, which resulted in Smith’s diagnosis of Parkinson’s Disease.
He and his wife, Susan, have been living with the disease - a chronic and progressive movement disorder - for nearly three years now.
As they've worked to maintain a quality of life for themselves, they've also been looking out for other sufferers of Parkinson's.
Ken Smith has been a leader in the sense of sharing his experiences and his knowledge, and providing others in the Greenville Area Parkinson Society (GAPS) peer group a chance to see the success you can have it you undertake certain types of therapies or if you do certain activities, said Tim Bishop, executive director of GAPS.
Both Ken and Susan are part of a movement to Strike Out Parkinson's.
That movement is an event happening on April 23 on Fluor Field. It will raise money to support the programs and services offered by the Greenville Area Parkinson Society (GAPS). The money raised offers education, support and therapy programs to the over 5,000 Upstate families affected by this disease.
Bishop describes the event as a "community awareness raiser."
"There's over 5,000 people with Parkinson's in the Upstate and most of them have no knowledge of the services we have available to them," Bishop said. "We want to grow and become much larger because we know there’s so much unmet need."
A big part of Strike Out, said Susan Smith, a volunteer on the Strike Out committee, is to encourage people that either have Parkinson's or a caregiver to come out and find out that there are resources.
The ability to access resources through peer support groups offered by GAPS was a reason the Smiths moved to Greenville from Michigan, though their son and grandchildren have lived here since 1998.
The couple lived in a small town in Michigan where they weren't close to hospitals and doctors and "there weren't support groups," Susan Smith said.
"When we heard about this in Greenville, we started to come. Once a month they have speaker meetings and then once a month they have the peer groups," she said. "It was a tremendous help because it’s educational. The speakers each month talk about a different aspect of Parkinson's."
The peer group, she said, is an opportunity for those with Parkinson's and their caregivers or spouses to share what's happening and how they're dealing with aspects of the disease.
Ken Smith, a retiree who has worked in manufacturing management and sales of engineer products, said the biggest thing that Parkinson's has done for him is given him fatigue and apathy.
He said about a year after he was diagnosed, he "finally got out of the denial stage and into the reality stage of it all."
He began to sink into depression.
"I had a very difficult time sleeping and I started losing weight," he said. "I was getting really down and out so I went back to my family doctor and he says, 'Ken we’re going to fix this.'"
Smith was placed on antidepressants and anti-anxiety medication. He finally feels like a human being again.
He encouraged members of his peer group to seek help if they think the same thing is happening to them.
"Don't let your pride get in the way. You have to do something," he said.
The conversation that Ken Smith is having with his peers is that "you can’t hide yourself away. You've got to connect and be with others because the depression and the anxiety can just become overwhelming," Bishop said. "This is a disease that doesn’t go away. It’s progressive but Ken is doing physical therapy, exercise classes, all the things you can do to slow it down."
There's a lot of home on the horizon with new medications and new treatment for Parkinson's Bishop said,and one day they'll find a cure.
"Until then, you've got to fight everyday," he said.
Susan Smith said in the caregivers group, which is predominately women at GAPS, "we encourage the other women to take care of themselves and get out if they can or get help so they can get out."
Some people with Parkinson's have progressed to where they need wheelchairs or a walker.
"Falling is a big thing with Parkinson's so some people are afraid to leave their spouses out of fear that they’ll fall or they’ll forget to take their meds," she said.
But, Ken Smith said, "the spouse as the caregiver needs to get away as best as he or she can in order to keep their sanity."
Parkinson's is different for everyone who has it, as far as how the symptoms manifest, Bishop said, but the one thing many of the patients have in common is the willingness to keep fighting.
"I am in awe of what all these individuals do to keep getting up every morning," he said. "I feel ashamed that I don’t do a lot of those things and I have a quality of life that they fight for everyday. So Strike Out Parkinson's is all about of celebrating what you can do with Parkinson's and to come together and learn how you can support each other and do more."
Strike Out Parkinson's will be from 10 a.m. to Noon.  There will be a walk, balloon release, music, informational booths for those who want to learn about Parkinson's and more.

Common Gene Variation May Predict Parkinson’s Severity and Progression, Study Reports

Margarida Azevedo

April 21, 2016

Researchers found a genetic variation, known as the GG genotype, that identifies those Parkinson’s disease (PD) patients more likely to have slower disease progression — evidenced through tremors — and lower levels of alpha-synuclein, a protein linked to the disease. The findings have implications in disease diagnosis and treatment strategies, and were recently presented at the 68th Annual Meeting of American Academy of Neurology in Vancouver, Canada.
Clinical evidence suggests that tremors seen as the initial or dominant Parkinson’s symptom, as opposed to balance and walking problems, point to a slower disease progression and lower risk of dementia onset.

Researchers at the Perelman School of Medicine at the University of Pennsylvania investigated single nucleotide polymorphisms (SNPs), genetic variations among the population that, when occurring within a gene or regulatory region near a gene, may affect its function with pathological consequences.

The GG genotype, a relatively common SNP near the alpha-synuclein (SNCA) gene, was found to be a predictor of disease severity.
Genotypes in a total of 251 PD patients were studied, with the focus on 10 PD-associated genetic variations and their influence on patients’ symptoms. Results revealed that 39 of the patients who had the GG genotype were more likely to have tremors, as opposed to balance and walking problems, slower physical disease progression, and lower levels of alpha-synuclein in the brain, the major component of Lewy bodies, a hallmark of PD that greatly contributes to neuronal death. The researchers performed the same analysis in another 559 patients at three other clinical sites in the U.S., finding similar associations between genotype and PD symptoms.

“This is how we can start thinking about precision medicine in action,” Dr. Alice S. Chen-Plotkin, MD, an assistant professor of neurology and the study’s senior author, said in a news release. “We found that a relatively common genetic variation can both serve as a biomarker for and influence the disease course of Parkinson’s patients. This opens up the possibility of achieving a hallmark of precision medicine: targeted therapies for different ‘versions’ of what was once thought to be a single disease.