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I have Parkinson's diseases and thought it would be nice to have a place where the contents of updated news is found in one place. That is why I began this blog.

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Friday, April 29, 2016

U.S. approves Acadia drug for Parkinson's disease-linked psychosis

Fri, 29 Apr 2016 

Acadia Pharmaceuticals Inc's drug for psychosis linked to Parkinson's disease was approved by the U.S. Food and Drug Administration on Friday, becoming the first ever treatment to get a U.S. nod for the condition.
The regulator, however, asked Acadia to include a black-box warning, its strictest warning, on the drug's label for an increased risk of death associated with its use in older people.
Analysts have said the warning will have a limited impact on sales as antipsychotics often come with such warnings. 
(Reporting by Subrat Patnaik in Bengaluru; Editing by Kirti Pandey)

10 Essential Facts About Parkinson's Disease

The movement disorder affects each person differently, but tailoring your treatment for specific symptoms can improve your quality of life.

Parkinson’s is chronic and progressive, affecting the nerve cells in the brain.

April 27, 2016

Parkinson's disease, a degenerative disorder of the central nervous system that affects nerve cells in the brain and makes movement difficult, affects an estimated one million people in the United States, according to the National Parkinson Foundation. The disorder is chronic and progressive, affecting the nerve cells that produce dopamine. When these cells become impaired or die, the loss of dopamine leads to abnormal nerve firings and impaired movements, including tremors, loss of balance, and other problems, explains the National Institute of Neurological Disorders and Stroke.

There is no cure yet for the condition, but researchers say they’re piecing together more clues about the roles of genetic and environmental factors. Meanwhile, those diagnosed can take many steps to protect their quality of life and enjoy family, career, and retirement.

If you or a loved one has recently been diagnosed, here are 10 essential facts you need to know:

1. Parkinson's disease is not just an ''old person's disease." While the disorder is typically diagnosed at around age 60, younger people can also be affected, says neurologist and movement disorder specialist Rachel Dolhun, MD, vice president of medical communications at the The Michael J. Fox Foundation for Parkinson’s Research. "People who are younger can get this," Dr. Dolhun says.

A prominent case in point is actor Michael J. Fox, now 54, who was diagnosed in 1991 at age 29, she says. "We call it young-onset Parkinson's at age 40 or under," Dolhun says. More typical, she says, is to be diagnosed in your 50s or 60s.

2. The cause of Parkinson's is still unknown. A combination of genetic and environmental factors are thought to contribute to the risk of getting Parkinson's, says Catherine Kopil, PhD, director of research programs for The Michael J. Fox Foundation. Several genetic mutations have been found that are linked to Parkinson's disease, and lifestyle may also play a role. Those who drink caffeine-containing drinks, for instance, have been found to have a lower risk of getting Parkinson's, although a cause-and-effect relationship has not been proven.

3. Diagnosing Parkinson's disease isn't simple. There's no specific test to diagnose Parkinson's disease. Instead, doctors look for four cardinal features of the movement disorder, says Hubert Fernandez, MD, the James and Constance Brown Family Endowed Chair in Movement Disorders and professor of medicine and neurology at the Cleveland Clinic Lerner College of Medicine in Ohio. His update on Parkinson's disease, focusing on what is new in diagnostic techniques and treatment, was published in September 2015 in the Cleveland Clinic Journal of Medicine. 
To diagnose the disease, doctors use the mnemonic TRAP:
Tremor or shaking at rest, involving the thumb, entire hand, arm, chin, lips, and feet
Rigidity felt by the doctor when rotating a patient's wrist or elbow
Akinesia or bradykinesia (lack of movement or slowness of movement) when walking or swinging an arm
Postural instability, making it necessary to hold onto something to maintain balance when walking or rising from a chair

Doctors must rule out other conditions, such as medications that cause the same symptoms, arthritis, or other medical issues. Observing symptoms, plus taking a medical history and asking patients if they feel stiff, slow, or shaky, is how the condition is typically diagnosed.

4. Parkinson's disease isn't just marked by tremors and other outward symptoms. While those outward symptoms are used as the basis for a diagnosis, the condition involves much more, Dolhun says. "There’s a lot that doctors can't see," she says, calling them the “invisible symptoms” that include sleep problems, constipation, slurred speech, and mood problems such as depression.
Symptoms vary from one patient to the next, Dolhun says. Indeed, there's an old saying, "If you’ve met one patient with Parkinson's, you've met one patient with Parkinson's."

5. Educating yourself about Parkinson’s can improve your quality of life. Good quality of life is possible ''if you seek good treatment and have a good plan," says Michael Okun, MD, national medical director for the National Parkinson Foundation and author of Parkinson's Treatment: 10 Secrets to a Happier Life.
Dr. Fernandez agrees and tells patients that Parkinson's, like high blood pressure, high cholesterol, and other chronic conditions, needs to be managed daily. "The more they know, the more they can advocate for themselves," says Fernandez, who coauthored Ask the Doctor About Parkinson's Disease with Dr. Okun.

6. Treatment should be tailored to your symptoms and your preferences. While there is as yet no cure for Parkinson's disease, treatment can help people live a good quality life. The primary treatment for the tremors and rigidity is a carbidopa-levodopa combination drug, like Sinemet and Rytary, which is thought to help replenish the lost dopamine. But symptoms of Parkinson's disease not only vary from patient to patient — patients also report that they aren't equally bothered by the same symptoms, Fernandez says. He always asks his patients: What bothers you most?
For some, he says, it's the constipation. Others tell him they're bothered by constantly shaking hands (tremor).
"The treatment plan should be tailored to the most pressing concern," Fernandez says.

7. Clinical trials are worth considering. Every time a Parkinson's disease patient visits their doctor, Okun suggests they ask, ''What's new? Am I eligible for any new clinical trial?'' Research is constantly evolving, so it's worth asking if any trials fit your situation.
"A lot of patients enrolled in clinical trials do better,'' he says, ''partly because they are seen more often." Every clinical trial has risks and benefits. There is a potential for harm or injury, but the trial researchers should be sure those risks are minimized in relation to the benefits. Enrolling may also give access to a treatment not otherwise available. Before enrollment, trial administrators should spell out the risks and benefits. 
Besides checking in with the doctor, anyone can look up clinical trials at, part of the National Institutes of Health. The Michael J. Fox Foundation site also has a trial finder feature that matches patients with appropriate trials.

8. Stress can make the condition worse; telling people about the condition can ease it. Stress can increase symptoms, Dolhun says. For some, one source of that stress is hiding the condition from coworkers, family, and friends, she says. "The majority of people we talk to who say they have shared their story with family and friends say they wish they would have done it sooner," she says.

9. Hospitalizations can be risky. Research has shown that patients with Parkinson's disease are at risk for getting the wrong medicine at the wrong time, and for contracting infections if they are hospitalized, which could lead to deterioration in their overall health. While hospitalization is sometimes necessary, Okun encourages patients to avoid hospital stays by keeping on top of their treatment plan and taking medicine as directed — and to get care in an outpatient center or medical clinic whenever possible.

10. Depression may affect more than half of all patients, and anxiety affects about 40 percent. Both anxiety and depression can affect the overall health of someone with Parkinson's even more than motor symptoms do, according to the National Parkinson Foundation. And depression and anxiety often occur together, according to research. Fortunately, treatment helps, and options ranging from exercise to medication and psychotherapy, or ''talk therapy,'' are plentiful.

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    Michael J. Fox slams reports about 'declining' health as he continues Parkinson's battle

    MICHAEL J. FOX has slammed "disturbing" reports about his "declining" health.

    The 54-year-old took to Twitter earlier today to hit out at claims made by US publication Globe, which suggested he had "refused to have life-saving surgery" and accepted "he has no hope of halting his Parkinson's disease".
    Sharing a screen shot of the tabloid's article, Michael posted: "Recent story in the Globe re my health and state of mind went viral. Disturbing and total B.S. The Globe apologizes."
    Michael learned he had Parkinson's disease back in 1991, before publicly announcing it after undergoing brain surgery to control his shaking in 1999.
    Speaking during a chat with David Letterman, Michael previously described the day he received his diagnosis.
    Recent story in the Globe re my health and state of mind went viral. Disturbing and total B.S. The Globe apologizes.

    Michael J. Fox Finds False Reports About His Health 'Disturbing and Total B.S.'


    Patient-Specific Stem Cell Therapy to Halt or Reverse the Damage of Parkinson’s Disease Gets Support from National Stem Cell Foundation

    29 Apr 2016 

    Summit for Stem Cell has received a $250,000 grant from the National Stem Cell Foundation (NSCF) to support the development of a patient-specific stem cell therapy for the treatment of Parkinson’s disease. The Summit research project is directed by Dr. AndrĂ©s Bratt-Leal in the lab of Dr. Jeanne Loring at The Scripps Research Institute in San Diego, CA. 
    The aim of of the research is to use a patient’s own skin cells to create normal dopamine-producing neurons that can be returned to the patient without rejection. Dopamine, a chemical that sends messages to areas of the brain that control movement and coordination, is decreased in Parkinson’s when dopamine-producing neurons malfunction or die. This patient-specific therapy has the potential to halt or reverse the damage of Parkinson’s disease and other neurological disorders, including ALS. 
    According to Dr. Paula Grisanti, National Stem Cell Foundation Chairman, “As an organization, we are committed to partnering with strong organizations and building consortiums to get great research through the funding “valley of death” that is too often the fate of promising ideas. We are delighted to make this grant for patient-specific stem cell research that will advance treatment options for Parkinson’s and other neurodegenerative diseases.” 
    Jenifer Raub, Summit’s Board President, says, 
    “The generous support provided by the National Stem Cell Foundation will advance this research at a critical point and move us closer to FDA-approved clinical trials. We are thrilled by this unique partnership with NSCF.”
    About Summit for Stem Cell 

    Summit for Stem Cell is an all-volunteer organization working to fund research that will directly impact treatment options for the debilitating effects of Parkinson's disease. Summit is at the vanguard of a unique collaboration between patients, clinicians, scientists, volunteers, patient advocates and the community-at-large to move innovative research forward in cooperation with The Scripps Research Institute and Scripps Clinic. For more information visit:

    About National Stem Cell Foundation 

    The National Stem Cell Foundation is a 501(c)3 non-profit organization funding stem cell and regenerative medicine research and clinical trials in four primary focus areas: Neurodegenerative Disease, Autoimmune Disease, Rare Childhood Disorders and Regenerative Repair. NSCF’s goal is to fund promising developments in the field of regenerative medicine, support research collaboration wherever possible and accelerate access to scientific breakthroughs for people in need. For more information visit:

    Mapping the thesaurus of the human brain

    Chris Wood  
    April 28, 2016

    The research reveals that at least a third of the brain's cerebral cortex is involved in processing language (Credit: UC Berkeley/Nature). 

    Researchers from the University of California, Berkeley (UC Berkeley) have used MRI data to create what they call a "semantic atlas," using vivid colors in multiple dimensions to show how the brain organizes language. The greater understanding that the map provides could one day help patients suffering from conditions such as motor neuron diseases and strokes in making themselves understood.
    Recently, we've seen some big developments in our understanding of exactly how the brain works, with scientists at Ohio State University working to pinpoint where in the brain we process facial expressions. Now, researchers from the University of California, Berkeley are tackling another big question – that of how we process language, creating a map that describes how the brain organizes words. 
    The new study involved seven participants listening to stories from the Moth Radio Hour – a public radio show – for two hours while remaining motionless inside an MRI machine. The blood flow in the patients' brains was measured as they listened with their eyes closed. That data then matched to time-coded transcripts of the stories, and finally through a word-embedding algorithm, scoring words according to how semantically similar they are to one another. 
    All that data resulted in a thesaurus-like map of the brain, with words arranged across the hemispheres of the brain, grouped under various headings such as tactile, visual, social or emotional.
    Studying the map reveals that at least a third of the brain's cerebral cortex is involved in processing language. The results also revealed that while everyone's brain is, of course, different, patients shared broadly similar language maps, with types of word arrayed in a roughly similar manner across the brains of the different participants.
    The knowledge of how the brain organizes words by meaning might actually have practical applications, possibly coming to the aid of people who have difficulty speaking, such as motor neuron disease patients or stroke victims. 
    Using the knowledge from the study, it's possible that doctors could one day track brain activity of patients that are unable to communicate, using the map to determine what the person is trying to say. 
    Looking forward, the researchers plan to increase the patient sample size in order to better understand the nuances of how we process words. 
    "Although the maps are broadly consistent across individuals, there are also substantial individual differences," said senior study author Jack Gallant. "We will need to conduct further studies across a larger, more diverse sample of people before we will be able to map these individual differences in details."

    Damaged gut flora linked to metabolic disorders, pioneering population study reveals

    April 28, 2016

    This site is copyright protected and I am unable to copy the information: To read the article go to:

    The findings represent microbiota composition of the general population. Previous studies have focused on specific diseases or featured a significantly smaller geographical scope.

    Acadia drug approval could clear way for Axovant dementia therapy

    REUTERS: An imminent ruling on Acadia Pharmaceuticals Inc's drug for Parkinson's disease psychosis is being closely watched by a Bermuda-based company with a similar treatment for dementia.
    Axovant Sciences Ltd's experimental drug for Lewy body dementia - after Alzheimer's, the most common form of progressive dementia - would benefit from the approval of Acadia's drug, Axovant's chief development officer told Reuters.
    The decision by the U.S. Food and Drug Administration is due by May 1. Analysts expect a positive ruling after the drug won the backing of an independent panel of experts.
    Both companies' drugs are designed to treat conditions that have no specific pharmaceutical therapy approved by the FDA. The drugs target the 5-HT2A receptor in the brain, which is linked with neuropsychiatric disturbances.
    But while San Diego-based Acadia's Nuplazid seeks to treat Parkinson's disease psychosis (PDP), Axovant is targeting an oft-misunderstood form of dementia that affects 1.4 million Americans.
    Lewy body dementia, or LBD, is characterized by a build-up of abnormal proteins called Lewy bodies in parts of the brain that control cognition, movement and behavior.
    Since the symptoms resemble those of better-known diseases such as Alzheimer's and Parkinson's, LBD is underdiagnosed.
    In fact, conclusive diagnosis is possible only after death; an autopsy of comedian Robin Williams found the condition.
    Dr. Lawrence Friedhoff, Axovant's chief development officer, said approval of Acadia's drug would open a regulatory pathway for a class of drugs that would also include his own company's treatment, called Nelotanserin.
    Since the meeting of the panel of experts on March 29, shares of Acadia and Axovant have risen about 25 percent and 17 percent respectively.
    "If Acadia is successful with Nuplazid, that would have a positive read-through for Nelotanserin," Friedhoff said in an interview. "It would suggest that we have a good chance."
    Friedhoff has decades of experience in the field. A former executive at Bristol-Myers Squibb Co and Eisai Co Ltd, he has sometimes been called the 'Father of Aricept' for his work in developing the top-selling drug for Alzheimer's.
    Nelotanserin is being tested in two mid-stage studies to treat visual hallucinations and REM sleep behavior disorder. The earliest the drug be approved is 2019, according to Axovant.
    Acadia's Nuplazid is expected to generate peak sales of US$300 million, according to data compiled by Thomson Reuters Cortellis.
    The potential for Nelotanserin is even greater.
    Piper Jaffray analyst Charles Duncan said the drug's addressable population was about quadruple that of Nuplazid as a treatment for Parkinson's disease psychosis alone. Acadia could also test its drug on LBD patients, he added.
    "Lewy body dementia is one of the most interesting, under-recognized disorders," said Duncan. "I suspect you'll see Acadia go there too."
    (Reporting by Natalie Grover in Bengaluru; Editing by Robin Paxton and Ted Kerr)

    Dopamine-making neurons can be chemically controlled in animal model of Parkinson's

    By Bradley J. Fikes 

    Genetic engineering makes stem cell-derived neurons amenable to fine-tuning

    April 28, 2016
    Dopamine-making neurons can be chemically activated or inhibited, according to research on a possible new Parkinson's therapy. — University of Wisconsin/Madison 

    Stem cell-derived neurons transplanted into the brains of Parkinsons' patients may be controllable by drugs after transplantation, according to research performed in a mouse model of the disease.
    If the work can be translated to humans, it would allow doctors to fine-tune the transplanted neurons to the needs of individual Parkinson's patients. However, it will take years before such a therapy can be tested in patients.
    The mice received human dopamine-producing neurons. These are progressively destroyed in Parkinson's disease, impairing movement. The replacement neurons, grown from pluripotent stem cells, were genetically engineered to alter dopamine production in response to a drug.
    The study was published Thursday in the journal Cell Stem Cell. The first author is Yuejun Chen, the senior author is Su-Chun Zhang; both of University of Wisconsin-Madison. When published online, the study can be found at:
    Transplants of fetal brain cells into Parkinson's patients illustrate why it's desirable to control these neurons after the operation, the study said. The results have been unpredictable: some patients have recovered the ability to move normally, while others experienced involuntary movements characteristic of an "overdose" of the cells.
    Researchers are trying to improve these results by making neurons from stem cells, a source that can be subjected to precise quality control. Carlsbad-based International Stem Cell Corp. recently began a clinical trial of its approach, which grows the neurons from cells produced from parthenogenetic, or unfertilized human egg cells.
    And a San Diego-based group called Summit for Stem Cell has grown dopamine-producing neurons from artificial embryonic stem cells called induced pluripotent stem cells. These cells are derived from the patients to be treated. The group has held preliminary talks with federal regulators. Before it can more forward, the group needs to raise millions to conduct the clinical trial.
    The study is sound, said Andres Bratt-Leal, Senior Scientist for Summit For Stem Cell, and the technology might eventually incorporated into the approach taken by the group. But first, Summit For Stem Cell must successfully test the transplant protocol it has already devised, Bratt-Leal said. Then the group can incorporate refinements.
    "It's a really neat trick that they did, and it's a really great research tool," Bratt-Leal said. "In terms of how it relates to our project, it's not something we would do the first go-around. It's something I could see groups using in version 2.0, after you have a cell therapy that you know that works."
    Version 1.0 will provide needed information to design the drug-controllable neurons, Bratt-Leal said. For example, it would be helpful to know the variation in individual response to the transplanted neurons.

    Scientists step closer to Alzheimer’s, Parkinson's cure

    New research showcases how scientists reversed symptoms of Alzheimer’s and Parkinson’s disease

    April 26, 2016      By Barry Eitel   SAN FRANCISCO

    A cure for Alzheimer’s and Parkinson’s disease is on the horizon after an international team of scientists successfully reversed symptoms, researchers announced Monday.
    The two diseases are caused by the deterioration of neurons, highly specialized cells in the brain and central nervous system. 
    Advanced Alzheimer’s disease results in the loss of memory, erratic behavior and death. Parkinson’s disease is not necessarily fatal, but results in disrupted motor skills, extreme tremors and loss of balance. 
    Scientists were able to destroy two different chemicals in the brains of fruit flies that reversed the symptoms of the two diseases. The chemicals are known as kynurenine pathway (KP) enzymes and are named kynurenine-3-monooxygenase (KMO) and tryptophan-2,3-dioxygenase (TDO).
    The team hopes that the discovery will lead to a breakthrough in the treatment of humans. While human brains are obviously much larger, they actually share many of the same genes as fruit flies. 
    The research was published Monday in the journal Proceedings of the National Academy of Sciences. Researchers were based at the University of Maryland School of Medicine and the University of Leicester in the United Kingdom. Funding came from the United States government through the National Institutes of Health. 
    "Our work strongly supports targeting of the KP as a potential treatment strategy for several major neurodegenerative disorders and suggests that alterations in the levels of neuroactive KP metabolites could underlie several therapeutic benefits," according to the study. 
    Alzheimer’s Disease International, a global non-profit, estimates that almost 44 million people across the planet have Alzheimer’s in 2016, but only a quarter of sufferers are diagnosed. Patient support non-profit Parkinson’s Disease Foundation believes 10 million people are living with Parkinson’s worldwide. 
    Scientists believe the study could also lead to a cure for Huntington’s disease -- a much less common degenerative brain disorder that effects behavior, movement and cognition skills.

    Study shows how neurons decline as Parkinson's develops

    April 27, 2016

    Electrical activity dwindles in cells long before movement issues become visible
    Michael Beckstead, Ph.D., of the School of Medicine at The University of Texas Health Science Center at San Antonio, and his colleagues conducted research that showed electrical activity dwindles in cells long before movement issues become visible. They documented the decline at several time periods in a mouse model.
     It's an unsettling thought: You could be walking around for 20 years developing Parkinson's disease and not even know it. 
    And once symptoms appear, it's too late for a cure.
    What if a therapy that treats the root causes of Parkinson's, not just the symptoms, could be started earlier?
    Researchers in the School of Medicine at The University of Texas Health Science Center at San Antonio are studying changes in Parkinson's-affected cells at various stages of the disease, long before any symptoms are evident. They describe the changes in an April issue of the Journal of Neuroscience.
    The hope of the research is twofold: 1) gain understandings that can be used to formulate a drug to arrest the disease at a halfway point, and 2) lengthen the time when patients with Parkinson's can lead healthy, productive lives.
    Hidden changes
    "For the first time we are getting a look at what's going on in the time window before the disease visibly takes hold but while changes are occurring," said study senior author Michael Beckstead, Ph.D., assistant professor of physiology and a member of the Barshop Institute for Aging and Longevity Studies at the UT Health Science Center. 
    Parkinson's is marked by the degeneration and death of cells called dopamine neurons. These neurons are found in a brain structure called the substantia nigra. The Health Science Center researchers studied mice in which only these neurons are affected by a genetic mutation.
    The MitoPark mouse, as it is called, is designed so that mitochondrial activity is hampered just in dopamine neurons of the substantia nigra. Mitochondria produce energy for our cells, and since these mice have impaired mitochondria, their dopamine neurons don't make energy efficiently.
    Mimics human Parkinson's
    At first, the mice are completely normal, but as weeks and months go by, the mutation causes their dopamine neurons to slowly become sick and die off. "It's a progressive model in that these changes don't take place overnight," Dr. Beckstead said. "This makes it like the human disease, which is thought to be somewhere in the range of a 20-year process before symptoms become evident."
    In MitoPark mice, behavioral symptoms such as tremor start to manifest when the mice are about 20 weeks old. The UT Health Science Center study assessed functional status at time points before that -- comparing dopamine neuron function at 6-10 weeks of age with function at 11-15 weeks of age and function at 16-plus weeks.
    Timeline of decline
    With these comparisons, the researchers constructed a timeline of functional decline in the dopamine neurons. They observed changes in three categories:
    * Smaller dopamine neurons * Reduced communication between the neurons * Impaired electrical activity of the neurons
    "Pretty much everything we measured declined in these cells," Dr. Beckstead said. "It was really remarkable how everything we studied changed. It was a general decline, and these changes were all occurring before the animals were symptomatic, before you could detect any sort of deficit in their movement."
    In older mice starting to display the abnormal movements of the disease, the scientists made another observation -- heightened gene expression to increase the electrical activity in the dopamine neurons. 
    "This is a late occurrence in the disease process," Dr. Beckstead said. "We believe the cells are trying to compensate for the declining electrical activity. That's probably how humans are able to be free of symptoms for so long when they have Parkinson's, even though 30 percent or more of their dopamine neurons have died out."
    The study results aren't going to translate into a clinical therapy any time soon, but such findings offer the promise that one day the root cause of Parkinson's may be understood and treated.
    Current treatments for Parkinson's disease are all symptomatic. They focus on improving the movement deficits and making the patients more comfortable. 
    "We don't have any treatments right now that actually affect the disease process," Dr. Beckstead said. "The reason we don't have any is we don't understand what's going on in the early stages of this disease. Studies such as ours will help fill in those knowledge gaps."
    Acknowledgments: Grants from the William and Ella Owens Medical Research Foundation, the National Institutes of Health and the U.S. Department of Veterans Affairs supported this work.
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