WELCOME TO OUR PARKINSON'S PLACE!

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.

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 AM NOT RESPONSIBLE FOR IT'S CONTENTS. I AM JUST A COPIER OF INFORMATION SEARCHED ON THE COMPUTER. PLEASE UNDERSTAND THE COPIES ARE JUST THAT, COPIES AND AT TIMES, I AM UNABLE TO ENLARGE THE WORDING OR KEEP IT UNIFORMED AS I WISH. IT IS IMPORTANT TO UNDERSTAND I AM A PERSON WITH PARKINSON'S DISEASE. I HAVE NO MEDICAL EDUCATION,

I JUST WANT TO SHARE WITH YOU WHAT I READ ON THE INTERNET. IT IS UP TO YOU TO DECIDE WHETHER TO READ IT AND TALK IT OVER WITH YOUR DOCTOR. I AM JUST THE COPIER OF DOCUMENTS FROM THE COMPUTER. I DO NOT HAVE PROOF OF FACT OR FICTION OF THE ARTICLE. I ALSO TRY TO PLACE A LINK AT THE BOTTOM OF EACH ARTICLE TO SHOW WHERE I RECEIVED THE INFORMATION SO THAT YOU MAY WANT TO VISIT THEIR SITE.

THIS IS FOR YOU TO READ AND TO ALWAYS KEEP AN OPEN MIND.

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Thursday, February 27, 2014

Nicotine Patches to Stop… Parkinson’s Disease? by MJF Foundation, FoxFeed Blog



Across the board, physicians agree: There’s no doubt that smoking is bad for you. But is it possible that there’s just something about a cigarette habit that might lower a person’s risk of developing Parkinson’s disease (PD)? Epidemiological data (in which patterns in comparative populations are analyzed) has long supported the ideathat those who have spent years as smokers don’t get PD as often as non-smokers.
Of course, smoking a pack a day to maybe prevent the onset of PD hardly makes sense — the adverse effects of puffing on nicotine cigarettes certainly outweigh any potential benefits. Still, the data on smoking and PD is too intriguing to ignore: looking collectively across many studies, it’s estimated that current smokers are 60 percent less likely to get PD than those who have never smoked. Which begs the question: Could there be a drug for PD hidden somewhere within the rolling papers? Researchers believe that maybe there is, and the potential therapeutic agent that they’re intrigued by is nicotine.
This month, an exciting development toward learning more about nicotine and PD: A clinical trial sponsored by The Michael J. Fox Foundation (MJFF) is launching in the United States to explore the potential therapeutic benefits of those very same nicotine patches that people take to try and quit smoking.
NIC-PD will enroll 160 PD patients in Germany and the U.S., providing some volunteers with nicotine patches and others with placebo patches, in order to determine if the real ones might have the potential to slow the progression of PD. Eighty of these patients will be enrolled at 11 centers in the United States, saysCornelia Kamp, the project manager of the American arm of the study.
“The drug used in the trial is the same exact drug from Novartis that people have used to quit smoking for many years,” explains Kamp, which is good news in terms of clearing hurdles associated with the therapy’s safety. She is hopeful that her team could have high level results from NIC-PD by spring of 2015. A best case scenario: The results both show that disease progression is slowed, and are convincing enough to encourage a larger follow-up study which could prove to be more definitive.
Of course, there are hurdles. Most imminently, explains the U.S. study Principal Investigator James Boyd, MD, of the University of Vermont, nicotine gets a bad rap with the public because of its relationship with tobacco and addiction. In smoking, it’s the bevy of chemicals in a cigarette and the process of smoking that can cause cancers, not the nicotine itself. Still, helping prospective trial participants, and PD drug developers alike, to understand its benefits could prove to be a challenge, due to nicotine’s reputation.
The good news for people with Parkinson’s, says Boyd, is that pre-clinical studies have shown that nicotine could protect dopamine-producing neurons in the brain from dying. But we’ve yet to see this effect in people. NIC-PD will be the first clinical study to begin to get to the bottom of this disease-modifying potential.
And there’s still much to learn about possible biological connections between nicotine and PD. To date, most human-based data around nicotine and Parkinson’s has been purely epidemiological, says Maurizio Facheris, MD, MSc. This means that there might be other ways to describe the relationship between nicotine and PD that aren’t “brain chemically-based.”
Here’s one such example of how epidemiological data can return scientific twists and turns: A past studyfrom Matthew Menza, MD, found that people with PD tend to be less likely on the whole to be “novelty-seekers,” possibly because they have less dopamine in the brain (dopamine might inspire people to be more likely to seek out emotional stimuli). These individuals were also more likely to see smoking as a bad idea. On the other hand, the study found, “novelty-seekers” were more likely to take risks such as smoking, and they were also less likely to develop Parkinson’s. In short: Maybe those who are in the early stages of PD are just less likely to smoke because of how their brains are wired.
The good news is, NIC-PD is designed to begin to clear up some of these questions, and determine if it’s the addition of nicotine in the body that could really be making the difference. In addition, MJFF is funding additional pre-clinical work to learn more about the biological potential of nicotine in the brain.
And there was more intriguing news from last January, when research published in Neurology, the medical journal of the American Academy of Neurology, found that a nicotine patch may improve the memory loss common in mild cognitive impairment (MCI), a condition that is often a precursor to Alzheimer's disease.
The next few years could be telling as to whether nicotine might help to slow or prevent PD. Stay tuned for updates.

And, please, in the meantime, says Facheris, remember, it’s never a good idea to light up if you can help it. The potential good in nicotine is always outweighed by the toxins that enter into the body when smoking a cigarette. That’s the stuff that could produce cancers.

You're all you have.






You're all you have.




Research shows that pesticides may increase risk of #Parkinson’s Disease. 











Research Identifies How Pesticides May Increase Risk of Parkinson’s Diseas

EMBARGOED FOR RELEASE UNTIL 4 PM ET, February 03, 2014

MINNEAPOLIS – New research shows how pesticides may increase the risk of Parkinson’s disease and that people with certain gene variants may be more susceptible to the disease. The research is published in the February 4, 2014, print issue of Neurology®, the medical journal of the American Academy of Neurology. The research shows that certain pesticides that inhibit an enzyme called aldehyde dehydrogenase (ALDH) are related to an increased risk of Parkinson’s disease. The enzyme plays a role in detoxifying substances in cells, along with metabolism of alcohol. The study also found that people with a variant of the ALDH gene were two to five times more likely to develop Parkinson’s disease with exposure to these pesticides than people who did not have that gene variant. “These results show that ALDH inhibition appears to be an important mechanism through which pesticides may contribute to the development of Parkinson’s disease,” said study author Jeff M. Bronstein, MD, PhD, of the David Geffen School of Medicine at UCLA and the Greater Los Angeles Veterans Affairs Medical Center and a member of the American Academy of Neurology. “Understanding this mechanism may reveal several potential targets for preventing the disease from occurring or reducing its progression.” The study involved 360 people with Parkinson’s disease in three rural California counties who were compared to 816 people in the area who did not have the disease. Researchers looked at participants’ exposure to pesticides at work and at home using a geographic computer model based on information from the California Department of Pesticide Regulation. The researchers developed a test to identify which pesticides inhibited ALDH. The 11 pesticides that inhibited ALDH, all used in farming, fell into four structural classes—dithiocarbamates, imidazoles, dicarboxymides and organochlorides. Exposure to an ALDH-inhibiting pesticide at both the workplace and at home was associated with increased risks of developing Parkinson’s disease, ranging from 65 percent for the pesticide benomyl to six times the risk for the pesticide dieldrin. People who were exposed to three or more of the pesticides at both work and home were 3.5 times more likely to develop Parkinson’s disease as those who were not exposed. Bronstein noted that the relationship between the gene variant and Parkinson’s only appeared when people had been exposed to the pesticides. “In other words, having this gene variant alone does not make you more likely to develop Parkinson’s,” he said. “Parkinson’s is a disease that in many cases may require both genetics and environmental factors to arise.” Bronstein said the findings provide several possible targets for lowering Parkinson’s risk, including reducing exposure to pesticides and improving the functioning of ALDH. The study was supported by the National Institute of Environmental Health Sciences, National Institute of Neurological Disorders and Stroke, Veterans Administration Healthcare System, Michael J. Fox Foundation, Levine Foundation and Parkinson Alliance. To learn more about Parkinson’s disease, please visitwww.aan.com/patients.
The American Academy of Neurology, an association of more than 27,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, concussion, Parkinson’s disease and epilepsy.
For more information about the American Academy of Neurology, visit http://www.aan.com or find us on FacebookTwitterGoogle+ andYouTube.

Sunday, February 9, 2014

SKIN DISORDERS IN PARKINSON'S DISEASE


8th February 2014 - New research

The integumentary system is the skin and its associated glands, including the sweat glands, the sebaceous glands, and the hair and nails. Those medical disorders asociated with the skin that commonly occur in Parkinson's Disease are seborrhea, hyperhidrosis, and melanoma.Seborrhea causes excessively oily skin. Sebaceous glands are glands in the skin that secrete sebum, to lubricate the skin and hair. Seborrhea can therefore result in excessive secretion of sebum by the sebaceous glands and its accumulation on the skin surface. There is an increased likelihood of seborrhea in Parkinson's Disease that is due to low dopamine. For more information go to Seborrhea

 Hyperhidrosis is overactive sweat glands. Hyperhidrosis can therefore result in excessive sweat secretion. There is an increased likelihood of hyperhidrosis in Parkinson's Disease. Instead of being due to Parkinson's Disease, the increased sweat secretion is usually due to Parkinson's Disease drugs. As an unintended side effect L-dopa can produce adrenaline, which stimulates the sweat glands. For more information go to Hyperhidrosis

Melanoma is a form of skin cancer. The risk of melanoma could sometimes be as much as four to five times higher in Parkinson's Disease. The melanocyes in the skin produce melanin, which is made from L-tyrosine via L-dopa. This is the same means as dopamine in the dopaminergic neurons. Given that melanin helps to protect skin cells from Ultra Violet induced damage, melanoma is probably increased in Parkinson's Disease because of the reduced capacity to produce L-dopa in the melanocytes.    

Monday, February 3, 2014

The Dream of a Pill Free Existence and the Continuous Dopaminergic Pump for the Treatment of Parkinson’s Disease

You can find out more about NPF's National Medical Director, Dr. Michael S. Okun, by also visiting the NPF Center of Excellence, University of Florida Center for Movement Disorders & Neurorestoration. Dr. Okun is also the author of the Amazon #1 Parkinson's Best Seller 10 Secrets to a Happier Life.

One of the common dreams shared by Parkinson’s disease patients around the globe is the possibility of living a pill free existence.  One cannot blame the Parkinson’s disease patient or caregiver for dreaming big.  A single day in Parkinson’s disease shoes is likely to reveal the need for dozens of pills administered day and night.   In many cases, pills are taken as frequently as every hour or two.  If you ask a Parkinson’s disease patient to place an entire pill regimen for the day into the palms of their hands, there is a better than average chance he or she will not be able to hold all of them.  Previously, there was a hope that deep brain stimulation may have offered the highly sought after “pill free existence,” however over two decades into its history, it is clear that in the majority of cases, medications will still be required.  There is however, another treatment strategy on the horizon.  A strategy that offers the possibility of constant stimulation of the brain’s dopamine receptors through the use of a continuous dopamine infusion pump technology.  In this month’s issue of Lancet Neurology the first randomized controlled trial of a continuous pump infusion technology for Parkinson’s disease has been published (online before print).

The trial utilized an intrajejunal (i.e. a tube inserted in the small intestine) levodopa-carbidopa intestinal gel pump infusion strategy, and it was designed to collect safety and effectiveness data.  The study was carefully conducted and was double blind (neither the patients nor the raters knew what was administered) and randomized.  It was conducted in 26 centers including Germany, New Zealand, and the US. Participants were randomized (1:1) to “immediate-release oral levodopa-carbidopa pills plus a placebo intestinal gel infusion or to levodopa-carbidopa intestinal gel infusion plus oral placebo pills.”  It is important to remember that everyone in the study received a pump, but half of the patients did not receive active therapy (through the continuous pump infusion). The authors were most interested in improving the amount of time spent in the “off state” following 4 months of therapy. Off-time improved by 4 hours in the pump group versus 2.1 hours in the pill group.  The amount of “on” time without troublesome dyskinesia was better in the pump group when compared to the pill group (4.1 vs. 2.2 hours).

The pump is approved and available in 43 countries.  The United States has lagged behind the world in adopting this new approach to Parkinson’s disease therapy.  However, in defense of the U.S.A. and the FDA, prior to the publication of the current pump trial, all previous results were based on uncontrolled evidence.  The benefits of the pump have been clearly demonstrated.  In this population of fluctuating patients, the data would suggest that the pump out-performs standard medical therapy.  The study did not enroll patients with severe dyskinesia, and it is unclear how the continuous infusion pump will perform in more severe and more disabled Parkinson’s disease patients.
One of the major drawbacks to the pump approach is the need for a percutaneous gatrojejunostomy (a small feeding tube).  These types of tubes can serve as nidus points for infections and other complications, and in the current study, device complications were present in 89% of subjects.  The complications were addressable in most cases, and were reported as lower than in previous pump trials.

Patients should be aware that the current version of the pump requires wearing an external device, and it also requires changing a dopamine cassette once or twice a day.  The dopamine cassettes are a little smaller than a cellular phone, and usually last about 14-16 hours.  Some patients will require two cassettes, and some will need additional medications during the bedtime hours.  The pumps require continuous maintenance and programming by a qualified professional.  The tube connected to the stomach also requires constant monitoring for infection.

If the continuous infusion approach receives FDA approval one important step will be to compare its effectiveness to that of deep brain stimulation therapy (DBS).  Patient selection for pumps versus DBS will be an immediate and critical unmet need.  One question will be whether the pump technology can help debilitated patients with and without cognitive dysfunction who may be excluded from DBS.

Patients should be aware that pumps are powerful symptomatic therapies, but not cures; and in most cases the continuous infusion pump will not address the dopamine resistant symptoms of walking, talking, and thinking.  Pumps have not been shown to delay disease progression.  The good news for the Parkinson’s disease community is that for a subset of patients a “pill free existence” may be on the horizon.

Posted: 2/3/2014 8:39:29 AM by Cathy Whitlock

Sunday, February 2, 2014

 This is a form to show that you are not intoxicated but have Parkinson's disease and your mannerism may look like you have had too much to drink.