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Welcome to Our Parkinson's Place


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
diseases as well and thought it would be nice to have a place where
updated news is in one place. That is why I began this blog.
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. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please no advertisers. This is a free site for all.
Thank you.


Saturday, October 10, 2015

ATCC to Develop Custom Cell Lines for The Michael J. Fox Foundation for Parkinson's Research

Delivering novel cell lines to researchers to speed discoveries for Parkinson's disease


MANASSAS, Va., Oct. 8, 2015 /PRNewswire/

 ATCC, the premier global biological materials resource and standards organization, announces today that it has been selected by The Michael J. Fox Foundation for Parkinson's Research (MJFF) to provide vital cell lines to academic, pharmaceutical, and biotechnology organizations committed to speed a cure for Parkinson's disease.

Parkinson's disease is a chronic, degenerative neurological disorder that affects one in 100 people over age 60. While the average age at onset is 60, people have been diagnosed as young as 18. Recent research indicates that at least 1 million people in the United States, and more than 5 million worldwide, have Parkinson's disease.
Under the terms of the agreement, ATCC will provide services and products to the global scientific community that is working to address this challenging disease.  Specifically ATCC will provide cell line authentication, mycoplasma testing, and repository management services.  ATCC will also produce and validate custom master cell banks (MCBs) from macrophage cell lines provided by MJFF, including wild-type LRRK2, LRRK2 knockout, and human LRRK2 T1348N (GTPase-dead) knockin.
"At our core, ATCC is about contributing to breakthrough scientific discoveries through the provision of high quality biological products and services.  We are honored to partner with The Michael J. Fox Foundation to accelerate breakthroughs in Parkinson's disease research," stated Raymond Cypess, DVM, Ph.D., CEO at ATCC.  "As the premier biological resource center that global researchers have relied on for 90 years, ATCC has been privileged to work with outstanding organizations, such as The Michael J. Fox Foundation, and we look forward to partnering with additional foundations."
Terina Martinez, Ph.D., associate director of research programs at MJFF, said, "These cell lines are important tools for our efforts to advance understanding of Parkinson's disease and further drug development toward new therapies for the millions living with this disease. We're pleased to be working toward these goals with ATCC, a well-regarded organization with the capabilities and track record to help us serve the Parkinson's research community."
This special cell line collection will be established by the end of the first quarter of 2016 and will be available at www.atcc.org.

About ATCC
ATCC collaborates with and supports the scientific community with industry-standard products and innovative solutions. With the world's largest and most diverse collection of human, animal, and plant cell lines, as well as molecular genomic tools, microorganisms, and biological products, ATCC is a trusted biological resource for the worldwide research community. Together, the people of ATCC share in its mission to acquire, authenticate, preserve, develop, and distribute biological materials and information for the advancement of scientific knowledge. Founded in 1925, ATCC is a non-profit organization with headquarters in Manassas, VA. Discover more at www.atcc.org.

About The Michael J. Fox Foundation for Parkinson's Research
As the world's largest nonprofit funder of Parkinson's research, The Michael J. Fox Foundation is dedicated to accelerating a cure for Parkinson's disease and improved therapies for those living with the condition today. The Foundation pursues its goals through an aggressively funded, highly targeted research program coupled with active global engagement of scientists, Parkinson's patients, business leaders, clinical trial participants, donors and volunteers. In addition to funding more than $450 million in research to date, the Foundation has fundamentally altered the trajectory of progress toward a cure. Operating at the hub of worldwide Parkinson's research, the Foundation forges groundbreaking collaborations with industry leaders, academic scientists and government research funders; increases the flow of participants into Parkinson's disease clinical trials with its online tool, Fox Trial Finder; promotes Parkinson's awareness through high-profile advocacy, events and outreach; and coordinates the grassroots involvement of thousands of Team Fox members around the world. 
Company contact 
Renee Randall  
ATCC
Tel: (703) 365-2773     

http://health.einnews.com/article/290590406/vuBpaUYTqhIFYygq

Scientists reveal 4 foods which could stop you getting cancer, Alzheimer's and Parkinson's disease

A natural compound found in each of the four foods could make a person's body less prone to age-related diseases, according to experts

Eating: Scientists say four foods, in particular, could help you beat cancer

Four foods with anti-ageing properties could help stave off cancer, Alzheimer's and Parkinson's diseases. 
That's the view of scientists behind a significant new study into cell matabolism. 
According to the experts, peas, blue cheese, corn and soybeans contain a natural compound called spermidine, which reverses the body's circadian rhythm.
This makes the body 'younger' and less prone to age-related diseases.
Dr Gad Asher, of the Weizmann Institute of Science in Israel, said: "This discovery demonstrates the tight intertwining between circadian clocks and metabolism and opens new possibilities for nutritional interventions that modulate the clock's function.
"Impaired circadian rhythmicity has been linked to a wide variety of age-related diseases, including cancer, Alzheimer's disease, Parkinson's disease, and inflammation."
Greens: Peas contain spermidine, which reverses the body's circadian rhythm
he study published in Cell Metabolism said polyamines, of which spermidine is an example, are essential molecules present in all living organisms that are derived from dietary sources and synthesised by our own cells.
They regulate a variety of key cellular processes such as cell growth and proliferation.
Dr Asher suspected that polyamines might also play a role in circadian biology because they are known to influence the clock's function.
Anti-ageing: Corn could make the body less prone to age-related diseases
When young mice were treated with a drug that inhibits polyamine synthesis, their circadian clock slowed down by about 11 minutes per day compared to untreated young mice.
On the other hand, adult mice that received extra spermidine in their drinking water had clocks that ran about eight minutes faster than untreated adult mice.
The effects of polyamines on the circadian clock were less pronounced in mice than in cells due to the tight regulation of these critical compounds in their natural physiological context.
Healthy: Soybeans were also listed among the four disease-beating foods 

However, even subtle clock deviations have been associated with a wide variety of metabolic and age-related diseases.
The crosstalk between circadian rhythms and metabolism may serve to fine-tune and reinforce the function of the clock, he added.
He said: "Our findings basically rely on experiments with mice and if they hold true in humans, they will have broad clinical implications.
"The ability to repair the clock simply through nutritional intervention, namely polyamine supplementation, is exciting and obviously of great clinical potential."
Surprise: Blue cheese isn't an obvious health food, but it could stave off disease
But Asher warned: "I would not recommend that old people rush out for anything, especially not to buy polyamines, until this is tested and proven in humans.
"Even if one consumes high amounts of polyamines, similar to many vitamins, an excess of them will simply not be absorbed or will be secreted in the urine unless the body is in need of them.
"But I do envision testing polyamines in clinical trials as a tool against a wide variety of age-related diseases in humans.
"There is evidence in flies and mice that polyamines extend lifespan, and future studies might also support the use of polyamines in humans."

http://health.einnews.com/article/290552358/eAZC2_JILKfmXU8I

Friday, October 9, 2015

Diet supplement keeps circadian clock from slowing down in aging mice


Published: 
Falling levels of polyamines, compounds present in all living cells, cause circadian rhythms to slow down in older mice, reports a study published October 8 in Cell Metabolism. This effect was reversed by dietary supplementation with a type of polyamine called spermidine, which is abundant in foods such as soybeans, corn, green peas, and blue cheese. No studies have yet been conducted in humans.
"This discovery demonstrates the tight intertwining between circadian clocks and metabolism and opens new possibilities for nutritional interventions that modulate the clock's function," says senior study author Gad Asher of the Weizmann Institute of Science. "Impaired circadian rhythmicity has been linked to a wide variety of age-related diseases, including cancerAlzheimer's diseaseParkinson's disease, and inflammation."
Polyamines are essential molecules present in all living organisms that are derived from dietary sources and synthesized by our own cells, and they regulate a variety of key cellular processes such as cell growth and proliferation. Asher and his collaborators suspected that polyamines might also play a role in circadian biology because they are known to influence the clock's function.
When young mice were treated with a drug that inhibits polyamine synthesis, their circadian clock slowed down by about 11 minutes per day compared to untreated young mice. On the other hand, adult mice that received extra spermidine in their drinking water had clocks that ran about eight minutes faster than untreated adult mice.
The effects of polyamines on the circadian clock were less pronounced in mice than in cells due to the tight regulation of these critical compounds in their natural physiological context. However, even subtle clock deviations have been associated with a wide variety of metabolic and age-related diseases. According to the authors, the crosstalk between circadian rhythms and metabolism may serve to fine-tune and reinforce the function of the clock.
"Our findings basically rely on experiments with mice, and if they hold true in humans, they will have broad clinical implications," Asher says. "The ability to repair the clock simply through nutritional intervention, namely polyamine supplementation, is exciting and obviously of great clinical potential."
But Asher urges caution for now. "I would not recommend that old people rush out for anything, especially not to buy polyamines, until this is tested and proven in humans. Even if one consumes high amounts of polyamines, similar to many vitamins, an excess of them will simply not be absorbed or will be secreted in the urine unless the body is in need of them," he says. "But I do envision testing polyamines in clinical trials as a tool against a wide variety of age-related diseases in humans. There is evidence in flies and mice that polyamines extend lifespan, and future studies might also support the use of polyamines in humans."
Age Related Decline of Polyamine
This graphic depicts how aging associated decline in polyamine levels lead to a correspondingly longer circadian period, which can be reversed by dietary polyamine supplementation.
Credit: Zwighaft et al./Cell Metabolism 2015
Adapted by MNT from original media release

http://www.medicalnewstoday.com/releases/300737.php?tw

Immune gene prevents Parkinson's disease and dementia

Published: 

An estimated seven to ten million people worldwide are living with Parkinson's disease (PD), which is an incurable and progressive disease of the nervous system affecting movement and cognitive function. More than half of PD patients develop progressive disease showing signs of dementia similar to Alzheimer's disease. A research team at University of Copenhagen, Denmark, has discovered that non-inheritable PD may be caused by functional changes in the immune regulating gene Interferon-beta (IFNβ). Treatment with IFNβ-gene therapy successfully prevented neuronal death and disease effects in an experimental model of PD. The results have just been published in prestigious scientific journal Cell.

Protein regulates waste management in nerve cells

The human brain consists of approximately 100 billion neurons, which coordinate activities in all parts of the body. At Biotech Research and Innovation Centre (BRIC), University of Copenhagen, the group of Professor Shohreh Issazadeh-Navikas has discovered that the immune gene IFNβ plays a vital role in keeping neurons healthy.
"We found that IFNβ is essential for neurons ability to recycle waste proteins. Without this, the waste proteins accumulate in disease-associated structures called Lewy bodies and with time the neurons die," explains assistant professor Patrick Ejlerskov, the first author of this report.
The research team found that mice missing IFNβ developed Lewy bodies in parts of the brain, which control body movement and restoration of memory, and as a result they developed disease and clinical signs similar to patients with PD and dementia with Lewy bodies (DLB).

New understanding of non-familial Parkinson's disease

While hereditary gene mutations have long been known to play a role in familial PD, the study from BRIC offers one of the first models for so-called non-familial PD, which comprises the majority (90-95%) of patients suffering from PD. 

According to professor Shohreh Issazadeh-Navikas the new knowledge opens new therapeutic possibilities:

"This is one of the first genes found to cause pathology and clinical features of non-familial PD and DLB, through accumulation of disease-causing proteins. It is independent of gene mutations known from familial PD and when we introduced IFNβ-gene therapy, we could prevent neuronal death and disease development. Our hope is that this knowledge will enable development of more effective treatment of PD," says professor Shohreh Issazadeh-Navikas.
Current treatments are effective at improving the early motor symptoms of the disease, however, as the disease progress, the treatment effect is lost. The next step for the research team will be to gain a better understanding of the molecular mechanisms by which IFN- protects neurons and thereby prevents movement disorders and dementia.

http://www.medicalnewstoday.com/releases/300796.php?tw

Researchers Report New Insights Into the Mechanisms Responsible for Slow Movements in Parkinson’s Disease

In a newly published paper in the Cerebral Cortex journal entitled “Dopamine D1 Receptor-Mediated Transmission Maintains Information Flow Through the Cortico-Striato-Entopeduncular Direct Pathway to Release Movements,” researchers from Japan reported that lack of dopamine transmission through D1 receptors is linked to slower movements in patients with Parkinson’s disease (PD).
Parkinson’s disease is a neurodegenerative disorder characterized by damaged motor neurons which control body movements. Patients with PD may suffer mainly from motor dysfunction like tremor, rigidity, postural instability, and slowness of movement. Other symptoms related to neuropsychiatry like trouble with speech, cognition, behavior, mood, thought, depression, sleep and memory commonly associated with dementia may arise. PD is assumed to be caused by genetic predisposition and environmental risk factors such as head injuries and exposure to pesticide and heavy metal commonly found in farming areas or in water sources. It is worth noting that PD affects around 0.3% of the total population in industrialized countries. The average age of onset of PD is around 60 years, and prevalence increases from 1% in people over 60 years to 4% in those over 80 years. PD invariably progresses with time and if not treated, motor dysfunction would progress aggressively in early stages of the disease, then slow down later.
It is believed that motor-related symptoms in PD result from death of dopamine-generating cells in the midbrain region called substantia nigra. Other studies suggested that dopamine binds to receptors D1 and D2. The latter have various effects on nerve cells located in brain region called basal ganglia. However, the mechanisms related to how dopamine controls information flow through these receptors and how this affects voluntary movements are still unknown. To clarify the issue, scientists from Japan performed a series of experiments using transgenic mouse model where dopamine D1 receptors could be reduced by mean of a pharmacological agent named doxycycline in a reversible way. The results illustrated that when D1 receptors were reduced, the mice suffered from decreased movements.
To gain a better understanding of the phenomenon, researchers examined the electrical activity of mice nerve cells in the brain region equivalent to globus pallidus in humans. In healthy mice, electrical stimulation of the motor neurons that lead to normal voluntary movements is expected to induce a response consisting of early excitation, inhibition and late excitation in the nerve cells, and inhibition is mediated by direct pathway to initiate movements. In the transgenic mouse where D1 receptors were decreased, a change in response to the electrical stimulation was observed and the inhibition stage responsible in initiating movement was significantly reduced. The latter highlighted the importance of dopamine transmission through mediation by D1 receptors in information flow as well as initiation of movement. Other data suggested that when D1 receptors were reduced, no change in spontaneous activity of nerve cells was observed. This does not support the view that lack of D1 receptor would increase spontaneous nerve cell activity. This means that what matters is the information flow through direct pathway to appropriately release motor action.
In conclusion, these findings revealed that lack of dopamine transmission through D1 receptors disturbs information flow through the direct pathway in motor neuron regions of the brain. The latter yields difficulties in initiating voluntary movements as in Parkinson’s disease. These findings could lead to the development of new therapies based on activation of D1 for PD and other related neurodegenerative diseases in the future.
http://parkinsonsnewstoday.com/2015/10/09/researchers-report-new-insights-mechanisms-responsible-slow-movements-parkinsons-disease/

Thursday, October 8, 2015

Breakthrough for electrode implants in the brain




Published: 
For nearly nine years, researchers at Lund University have been working on developing implantable electrodes that can capture signals from single neurons in the brain over a long period of time - without causing brain tissue damage. They are now one big step closer to reaching this goal, and the results are published in the scientific journal Frontiers in Neuroscience.
This technology would make it possible to understand brain function in both healthy and diseased individuals.
"There are several elements that must go hand in hand for us to be able to record neuronal signals from the brain with decisive results. First, the electrode must be bio-friendly, that is, we have to be confident that it does not cause any significant damage to the brain tissue. Second, the electrode must be flexible in relation to the brain tissue.
Remember that the brain floats in fluid inside the skull and moves around when we, for instance, breathe or turn our heads.
The electrode and the implantation technology that we have now developed have these properties, which is unique", says Professor Jens Schouenborg who together with Dr Lina Pettersson led the project.
The Lund researchers' tailored electrodes, which they call 3-D electrodes, are unique in that they are extremely soft and flexible in all three dimensions, in a way that enables stable recordings from the neurons over a long time.
The electrode is so soft that it deflects against a water surface. In order to implant such electrodes, the researchers have developed a technique for encapsulating the electrodes in a hard but dissolvable gelatine material that is also very gentle on the brain.
"This technology retains the electrodes in their original form inside the brain and can monitor what happens inside virtually undisturbed and normally functioning brain tissue", says Johan Agorelius, a doctoral student in the project.
Until now, developed flexible electrodes have not been able to maintain their shape when implanted, which is why they have been fixated on a solid chip that limits their flexibility, among other things. Other types of electrodes that are used are much stiffer. The result in both cases is that they rub against and irritate the brain tissue, and the nerve cells around the electrodes die.
"The signals then become misleading or completely non-existent. Our new technology enables us to implant as flexible electrodes as we want, and retain the exact shape of the electrode within the brain", says Johan Agorelius.
"This creates entirely new conditions for our understanding of what happens inside the brain and for the development of more effective treatments for diseases such as Parkinson's disease and chronic pain conditions than can be achieved using today's techniques", concludes Jens Schouenborg. 
Facts about the electrodes:
The electrodes are made of 4 μmgold leads and individually insulated with 4 μm parylene. The array of electrodes consists of eight flexible channels, designed to follow the movement of the brain.
Both the electrode and implantation technology, which have been tested on rats, are patented by NRC researchers, in Europe and the US, among other places.
http://www.medicalnewstoday.com/releases/300714.php?tw

Unexpected connections: Calcium refill mechanisms in nerve cells affects gene expression

Published: 
Researchers at the National Centre for Biological Sciences, identify new roles for calcium refill mechanisms in regulating dopamine in the brain
SOCE-Requiring Dopaminergic Neuron Clusters (Green) of the Flight Circuit in Drosophila Brain
These are dopaminergic neuron clusters (green) of the flight circuit requiring Store-operated Ca2+ Entry (SOCE) in the protocerebrum of an adult Drosophila brain. The brain neuropil is marked by anti-bruchpilot immunostaining (magenta). 
Credit: Trayambak Pathak
Calcium is not just required for strong bones - it is an essential requirement for muscle and nerve cells to work normally. Latest research from the National Centre for Biological Sciences (NCBS, Bangalore), now shows that maintaining Calcium balance in cells is also needed for another purpose - it may be regulating the levels of an important signalling molecule called dopamine in the brain.
Current work from Prof. Gaiti Hasan's lab at NCBS has identified new roles for Calcium signalling. Prof. Hasan's group show that a process called SOCE (Store Operated Calcium Entry) which works to maintain calcium levels in cells could also play a role in maintaining the levels of dopamine, a vital neurotransmitter in the brain.
SOCE is a process by which Calcium ions slowly enter cells to refill Calcium stores that have been depleted by various activities. Since the cell membrane or the outer covering of the cell is impermeable to Calcium ions, Calcium enters the cell through dedicated calcium channels. One such Calcium channel is a protein called Orai, which is an indispensable requirement for SOCE to work. Prof. Hasan's work used Drosophila flies with mutated Orai genes that prevented normal operation of the SOCE process. A key finding in their experiments was that when SOCE was inhibited only in certain neurons before the flies matured, the emerging adults could not fly. With no SOCE, the wiring process to create a 'flight circuit' in the fly brain did not develop - so, why is this important?
The importance of this result is that it revealed a potential link between SOCE and the neurotransmitter called dopamine. Dopamine is an indispensable signal molecule in the brain, whose deficiency causes various diseases, the most famous of them being Parkinson's syndrome. In the flightless Orai mutant flies, SOCE was inhibited in a set of cells called 'dopaminergic interneurons' - nerve cells that used dopamine to relay signals. Further investigations into this phenomenon revealed that SOCE and its role in maintaining Calcium levels within nerve cells affected processes related to dopamine synthesis and transport at a genetic level.
"We expected that inhibiting calcium refill via SOCE in nerve cells would impair their functioning and perhaps ultimately kill them. It was quite a surprise when we discovered instead that the SOCE process was affecting the level of enzymes required for synthesizing dopamine. The bigger surprise was that this phenomenon was occurring at the level of gene expression", says Trayambak Pathak, who is the first author on the publication which has appeared in the Journal of Neuroscience.
The implications of this work are intriguing. If SOCE operates similarly in mammalian cells, it might have some role to play in diseases where dopamine plays a significant role such as Parkinson's, Attention Deficit Syndromes (ADS) and even schizophrenia. "There is still so much more to understand in these processes. Our work has opened up a plethora of questions about the importance of SOCE in nerve cells. It may even provide us with new pathways to explore for treatments of conditions such as Parkinson's disease", says Prof. Hasan. 
Adapted by MNT from original media release
http://www.medicalnewstoday.com/releases/300721.php?tw

What it feels like to have Parkinson’s disease

  OCT 6, 2015
Jon Palfreman


In 1985, science journalist Jon Palfreman investigated a group of drug addicts who were struck with Parkinson’s-like symptoms after taking tainted heroin.
Thirty years later, Palfreman was diagnosed with Parkinson’s disease himself. His book, "Brain Storms," describes his journey with the disease and new treatments for patients. 


“Initially I denied [my diagnosis] and sought second opinions. I got pretty angry. I tried to keep it secret for a while, just like Michael J. Fox did,” Palfreman says, “It took me, I’d say, about a year before I really processed it properly and then I realized that I had a destiny to use my training as a science journalist and my insights as a patient to explore this malady, which was now going to be part of my life.” 

About 60,000 people each year in the US alone are diagnosed with Parkinson's disease. Palfreman says the malady means many things that he used to do automatically, now come with much more difficulty. 

“It is very much like getting on a plane and going to London and renting a car. You can drive on the left-hand side of the road, but you have to use your conscious brain to pay attention. Everything's a bit harder. When I walk, I have to sort of consciously move my arms back and forth. Whereas, when a healthy person does it, it's automatic. And so a lot of things that you got for free you have to work at,” Palfreman says. 

The disease has three stages. The first noticeable symptoms are subtle, such as a loss of smell, constipation and possible sleeping disorders. After that, the disease attacks a person’s ability to move. The third stage produces cognitive impairment and hallucinations. 

“What we classically think of Parkinson’s — the tremor, the slowness, the rigidity, the stooped gait — is really the middle act of a three-act play and that, basically, the diseases present maybe 10 or 15 years before a person gets diagnosed,” Palfreman says. “It's a much more systemic disease than it was once thought to be.”

There are several new treatments for the disease Palfreman has been watching. One of them is based on the theory that the disease is caused by a protein, alpha-synuclein, going rogue, forming clumps called amyloids, and jumping from cell to cell, killing cells in their wake. 

“If alpha-synuclein is causing all the problems, then trying to reduce the levels of it makes perfect sense, and in the next year or two, going into clinical trials, there are a number of products which are designed to sort of dissolve alpha-synuclein,” Palfreman says. “If they work, I mean the prospects are amazing. Somebody who didn't have the disease, if you can get in early enough, would never develop the motor symptoms. And somebody like me who had the motor symptoms could possibly be stabilized so it didn't get any worse. So there's a lot of excitement at the moment around this.” 

Palfreman says there are other things people with Parkinson’s can do to control the disease. 
“The one thing which really everybody should do is regular exercise because people who do exercise and stay mobile, they do much, much, much better than people who withdraw or give up,” Palfreman says. “Because you've still got the conscious part of your brain, you can still drive like you're driving into London on the wrong side of the road. It just takes a bit more energy and effort, but it still works.”

In the future, Palfreman predicts medical specialists will develop more advanced ways to control the disease.  

“Just like we have very sophisticated heart pacemakers, we might get a situation where I might get an electrode in my brain and, just before my my left hand wants to set off a tremor it sets off a pulse and reboots that part of the brain. And I think these things are pretty promising so that even if you haven't got a total cure, the management thing will become much better and we’ll be able to live pretty much essentially normal lives.”

http://kgou.org/post/what-it-feels-have-parkinson-s-disease#stream/0