I Ask This Of You!

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.

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. I will not accept any information about Herbal treatments curing Parkinson's, dementia and etc. It will go into Spam.

This is a free site for all with no advertisements.

Thank you for visiting!

Saturday, November 28, 2015

Adelaide Parkinson's pair tackle Everest Base Camp to break through limitations of disease

Never tell Mike Hannan and Heiko Maurer the limitations of having Parkinson's disease — they will try to climb Mount Everest to prove you wrong. 
"Most people with Parkinson's think they are incapable of exercise and doing strenuous things and their carers reinforce that," Mr Hannan said.
"Their view is the patients should sit in the corner and knit."
After more than a year of planning, Mr Hannan, Mr Maurer and Mr Hannan's daughter Katie began their trek to Everest Base Camp, 5,380m above sea level, on October 19.
PHOTO: Mike Hannan reached an altitude of 4,000 metres before he pulled out of the trek.

We wanted to show that just because you have Parkinson's it doesn't mean that it is an end to useful and productive life," Mr Maurer said.
At 74, Mr Hannan is at an age when most would be winding down.
"We thought it was a loony idea, but let's try it," he said.
"If we could show that we could get there, or partly there, and have a good time, it would show people that they needn't sit at home and be miserable."
The team set out hoping to raise $10,000 for Parkinson's research and the Shake It Up Foundation.

Up and downs of Parkinson's on the trip

Struggling with balance problems, a combination of his Parkinson's disease and the high altitude, Mr Hannan pulled out two days into the seven-day walk after reaching an altitude of 4,000 metres.
Mr Maurer, 61, continued, accompanied by Ms Hannan, 37, and both made it to Base Camp.
"It was the hardest thing I have done in my life," Mr Maurer said.
"There was a sense of accomplishment when I got there, but the reality of Parkinson's also hit home."
The elation of making the trek was balanced with the emotions of him facing his future with the disease.
"This is as good as it is going to get and from here it is downhill," Mr Maurer said.
Reflecting on the trip after returning to Adelaide, he said his pride of achievement had been replaced by the sadness of his situation.
"It's a one-time achievement, but the Parkinson's is with me for the rest of my shortened life."

Putting value on family, real-world experiences

Ms Hannan said accompanying her father and Mr Maurer was challenging beyond expectation.
As Mr Hannan began to reach his limit, she became worried about his welfare.
"I got quite scared and thought potentially he was not going to make it, and we were going to have to put him on a yak or carry him up there," she said.

The complications of his Parkinson's, paired with the low-oxygen environment, made her father's disease more aggressive.

Mike Hannan, Katie Hannan and Heiko Maurer back in Adelaide.

"When you have somebody in your family who you are close to, who is a friend as well, and you see them really struggling [it's really hard]," Ms Hannan said.
The trek provided some unexpected changes for Ms Hannan too.
A normally busy person, she said she had begun to concentrate more on the things she felt were important.
"I've started to say no to a lot of things," she said.
"I deleted the Facebook app on my phone yesterday and am trying to put a lot more value on real-world experiences.
"It's been unbelievable."

Setting new goals

Happily back in Adelaide, Mr Hannan said he would be keen to attempt the trek again.
"I would chose a different route though," he said.
"When you go to Base Camp you concentrate on getting there and getting back and you don't spend much time looking around," he said.
Mr Maurer said he was already eyeing off a trekking trip to New Zealand for his next adventure.

Scientists record real-time dopamine release in Parkinson's patients

November 28, 2015

New York: Scientists have reported first-ever measurements of a key neurotransmitter involved in learning with unprecedented precision in the brains of people with Parkinson's disease.

The measurements, collected during brain surgery as the conscious patients played an investment game, demonstrate how rapid dopamine release encodes information crucial for human choice.

The findings may have widespread implications not just for Parkinson's disease but for other neurological and psychiatric disorders as well, including depression and addiction, researchers from Virginia Tech Carilion Research Institute noted.
The researchers detected changes in the levels of dopamine a thousand times faster than had previously been recorded in humans.
These rapid measurements, combined with enhanced chemical specificity, led the scientists to discover that dopamine - a crucial neurotransmitter involved in learning and decision-making - has a far more complex role than formerly thought.
“More than 20 years of research in nonhuman model organisms has painted a very specific picture of the suspected role of dopamine in guiding human behaviour,” said Read Montague, director of the Human Neuroimaging Laboratory at the Virginia Tech Carilion Research Institute and senior author of the paper.
“And now, with these first-of-their-kind measurements, made directly in humans, we've discovered that this picture was woefully incomplete,” Montague noted.
Seventeen patients volunteered to allow Montague's team to record their dopamine signals during implantation surgery.
“Parkinson's disease is characterised by the death of dopamine-releasing neurons and we are trying to understand the underlying mechanisms of the disease process,” added Ken Kishida, first author of the paper and a research scientist.
The findings also have implications for understanding other disorders of the dopamine system.
“These precise, real-time measurements of dopamine-encoded events in the living human brain will help us understand the mechanisms of decision-making in health and disease,” the authors noted in a paper published in the journal Proceedings of the National Academy of Sciences.

Friday, November 27, 2015

Research paves way for clinical trials of cell therapies to treat Parkinson's disease, spinal cord injury

Published on November 26, 2015 

Stem cells that have been specifically developed for use as clinical therapies are fit for use in patients, an independent study of their genetic make-up suggests.
The research - which focused on human embryonic stem cells - paves the way for clinical trials of cell therapies to treat conditions such as Parkinson's disease, age-related degeneration of the eyes and spinal cord injury.

The study also sets out a cost-effective approach for monitoring the quality of stem cell-based products and newly emerging cell therapies.
Stem cells have the potential to become any of the varied cell types found in the body. Researchers have been investigating how they may be used to repair or replace damaged tissues in patients.

However, because the cells continuously produce copies of themselves, there are concerns that they may acquire genetic abnormalities that could lead to cancer.
Scientists at the University of Edinburgh investigated the genetic make-up of human stem cells that have been grown in the laboratory from cells found in the early embryo.

The 25 cell lines tested were all 'clinical-grade' - which means they meet the strict quality requirements for cell lines earmarked for use as therapies.
The team at the Medical Research Council Centre for Regenerative Medicine analysed each of the cell lines using a technique called molecular karyotyping, which is a highly sensitive method of detecting genetic abnormalities.
More than half of the cell lines carried large but stable genetic differences, the researchers found. However, these changes are also present in healthy people without significant consequences, reflecting the genetic diversity of the human population.continued genetic testing of emerging stem cell-based products to ensure they are suitable for use in patients.

The study is published in the journal Scientific Reports. It was funded by the Medical Research Council and The Cure Parkinson's Trust.
More than three-quarters of the global clinical-grade embryonic stem cell lines have been established the UK. The stem cell lines analysed in the study were established for clinical use by the Universities of Sheffield and Manchester, King's College London, and Roslin Cells, a company that specialises in the production of clinical-grade cells for use in therapies.

Dr Tilo Kunath, Senior Research Fellow at the Medical Research Council Centre for Regenerative Medicine, University of Edinburgh, said: "This is the largest study of therapeutically useful stem cells to date and shows that we are in a good place to push forward new cell therapies into clinical trials."

Dr Paul Colville-Nash, Programme Manager for Stem Cell, Developmental Biology and Regenerative Medicine at the MRC, said: "Collating a library of stem cells that we understand and know are fit for use in patients is vitally important if these are to be routinely used in the clinic. This work complements that of the UK Regenerative Medicine Platform that is seeking to address the key knowledge gaps needed to accelerate development, and ensure the safety and efficacy, of emerging stem cell therapies."
University of Edinburgh

Impax's NUMIENT granted EC marketing authorization for symptomatic treatment of adult patients with Parkinson's disease

November 25, 2015 

Impax Laboratories, Inc. (NASDAQ: IPXL) today announced that the European Commission (EC) has granted marketing authorization for NUMIENT (Levodopa and Carbidopa), a modified-release oral capsule formulation for the symptomatic treatment of adult patients with Parkinson's disease. The review of this application was conducted under the centralized licensing procedure as a therapeutic innovation, and is applicable in all 28 member states of the European Union, as well as Iceland, Liechtenstein and Norway.

"We are pleased that NUMIENT was approved by the European Commission as this not only showcases our R&D capabilities outside the US but is an additional positive review of our quality systems by another regulatory authority," said Fred Wilkinson, President and Chief Executive Officer of Impax. "NUMIENT addresses one of the most significant unmet needs for patients living with this disease, which is to reduce the amount of time during the day when their symptoms are not adequately controlled."

"This is our first branded drug approved for commercialization outside the United States and we are in active discussions with potential partners to support the commercialization of NUMIENT in Europe and the rest of the world. We are analyzing the options that will help facilitate the introduction of this product into the global market," concluded Mr. Wilkinson.

The EC decision is based on results from three Phase 3 controlled clinical studies which assessed the safety and efficacy of NUMIENT in patients with early (levodopa-naive) and advanced Parkinson's disease in the U.S. and in Europe.

Men's brains age FASTER than women's - making them more likely to develop diseases such as Parkinson's

Among men grey matter declined at a faster rate than women as they age

  • Men lost more matter in areas of the brain which deal with movement
  • Difference was 'striking' and could inform treatment of other disorders 

Among men grey matter in their brain declines at a faster rate than women as they get older, a study found
Among men grey matter declined at a faster rate than women as they get older, a study found.
Men also lost more matter than women in the caudate nucleus and the putamen volume, which deal with movement.
The study authors said that the difference was ‘striking’ and might inform treatment on other neurological disorders like ADHD.

The neuroscientists from the University of Szeged in Hungary scanned the brain structures of 53 men and 50 women.
The average age of the participants was 32, with the youngest participant being 21 years old and the eldest 58.
In their report, published in the journal Brain Imaging and Behaviour, the researchers found several differences between the sexes in their subcortical brain structures.

These are the parts of the brain that deal with not just movement but also emotional processing.
As men got older these areas showed a decline that was greater than among women.
Another part of the brain which showed a similar trend was the thalamus, which is like the brain’s main relay station for passing information around the brain.
Previous studies have said that men are twice as likely than women to get Parkinson’s, which affects around 127,000 people in the UK - but they did not say why.
The finding may explain why they are more susceptible to neurological conditions like Parkinson’s (file photo)

In their report the authors said that it could be due to changes in hormone levels as people got older and how the brain responded to these changes.
They wrote: ‘Strikingly, grey matter volume decreases faster in males than in females emphasizing the interplay between aging and gender on subcortical structures.
‘Changes of subcortical structures have been consistently related to several neuropsychiatric disorders (e.g. Parkinson’s disease, attention deficit hyperactivity disorder, etc.).
‘Understanding these changes might yield further insight in the course and prognosis of these disorders.’
Previous studies have shown that men have larger brains than women but this does not mean they are smarter - elephants and whales have bigger brains than humans.


27th November 2015 - 

Epidemiological studies previously reported a 60-70% reduced risk of Parkinson's Disease in smokers as compared to non-smokers. However, relationships between former smoking and Parkinson's Disease have been poorly investigated.
When assessed, current smokers were found to be far less likely to have Parkinson's Disease. Former smokers were found to be far more likely to develop Parkinson's Disease than people who had never smoked. Around 44% of people with Parkinson's Disease reported quitting smoking before they were diagnosed with Parkinson's Disease. The average time for cessation was 9 years, with a range of 2 to 16 years. The most important reasons given by people with Parkinson's Disease for quitting smoking were an illness different from Parkinson's Disease (51%), and knowledge of the harmful effects of smoking (47%).
The reduced prevalence of current smokers among people with Parkinson's Disease is consistent with previous findings, suggesting a protective effect of smoking. However, it could be due, at least in part, to the increased prevalence of former smokers among people with Parkinson's Disease patients, that were more prone to quit smoking.

Reference : Parkinsonism Related Disorders [2015] 21 (3) : 216-220 (M.Moccia, R.Erro, M. Picillo, E.Vassallo, C.Vitale, K.Longo, M.Amboni, G.Santangelo, R.Palladino, A.Nardone, M.Triassi, P.Barone, M.T.Pellecchia)
Complete abstract :
©2015 Viartis 

Wednesday, November 25, 2015

Exercise in Older Parkinson’s Patients May Lower Risk of Falling

November 25, 2015
Study shows 3 months of power training and yoga improved physical movement

Exercise can be a powerful prescription for improving movement in Parkinson’s disease (PD) patients. Researchers, trying to pinpoint those exercises that might best quell PD symptoms, recently reported that both power training and yoga were helpful to older people with PD. Their study, titled “Comparative Impact of Power Training and High-Speed Yoga on Motor Function in Older Patients with Parkinson’s Disease,” appeared in the journal Archives of Physical Medicine and Rehabilitation.
In PD, death of dopamine-producing neurons in a brain region called the substantia nigra causes problems with movement, rigidity and tremors. PD patients may experience falls, a particularly worrisome problem for older individuals. Medication and other treatments tend to focus on replacing the lost dopamine, and are not a cure. Exercise as an additional therapy can help to improve physical activity in people with PD, especially in easing symptoms like loss of balance or gait that leads to falls.
The study, led by Meng Ni of the Laboratory of Neuromuscular Research and Active Aging, University of Miami, included 42 PD patients, age 60 to 90, with an average age of 72. The study’s subjects had fallen at least once in the past year as a consequence of the disease. Researchers assigned participants to either high-speed power training, specifically designed yoga (both on a twice-weekly schedule) or no exercise for 12 weeks. Several standard tests were used to measure improvements, including overall PD movement symptoms via the Unified Parkinson’s Disease Rating Scale (UPDRS). They also assessed balance, reach, leg stance, posture, walking speed and leg press.
Both exercise groups improved in all of the physical tests except for reach (on the most affected side of the body), stance, and posture. Both yoga and power training were equally effective. The investigators noted, “Our three month, twice-weekly PWT and YOGA programs were able to alleviate motor symptoms, improve balance function and gait, and increase leg muscle strength and power in patients with mild to moderate PD. These two training systems should be considered viable interventions in rehabilitation programs designed to translate improvements in physical function into improvements in functionality and reductions in fall probability.”
Although it may be assumed that better physical fitness reduces the likelihood of falling, the study did not specifically address whether study participants experienced reduced falls. Further study of the exercise program could help to establish this. Still, based on these results, physical exercise appears to be helpful for older people suffering with PD.

Slower aging may protect cells in the brain from Parkinson's disease

Humans have long sought to reduce the effects of aging. Now, there may be another reason to continue searching for ways to slow the clock--preventing Parkinson's disease.
Scientists at Van Andel Research Institute (VARI) have shown in disease models that slowing aging reduces degeneration related to Parkinson's. The study was published online Nov. 19 in npj Parkinson's Disease, a new journal from Nature Publishing Group.
Parkinson's disease is the second most common neurodegenerative disorder and affects seven to 10 million people worldwide. Symptoms include slowed movement, resting tremor, postural instability and rigidity, as well as non-motor issues such as dementia, loss of sense of smell, sleep disturbances, constipation and depression.
"It is unknown why symptoms take many decades to develop when inherited mutations that cause the disease are present from birth," said Jeremy Van Raamsdonk, a VARI assistant professor and the study's senior author. "Aging is the greatest risk factor for developing Parkinson's--we believe changes that occur during the aging process make brain cells more susceptible to disease-causing mutations that don't cause issues in younger people."
In the brain, Parkinson's is marked by the dysfunction and death of the nerve cells that produce dopamine--a chemical that plays a key role in many important functions, including motor control. Clumps of a protein called alpha-synuclein also are found in brain cells of most people with Parkinson's, although scientists are still trying to pin down their exact role.
As part of their search for ways to prevent the disease, Van Raamsdonk's team delayed the aging process in genetic models of Parkinson's disease. They demonstrated that slower aging imparts protection against the loss of dopamine-producing cells in the brain and decreases the formation of alpha-synuclein clumps - both hallmark features of Parkinson's.
"This work suggests that slowing aging can have protective effects on the brain cells that otherwise may become damaged in Parkinson's," Van Raamsdonk said. "Our goal is to translate this knowledge into therapies that slow, stop or reverse disease progression."

Slowing aging, preserving brain cell function

In the study, Van Raamsdonk and his team used the worm Caenorhabditis elegans as a genetic model for Parkinson's. Thanks to its simple and well-mapped nervous system, and the ease of genetic manipulation and maintenance of the worm, C. elegans is well-suited for the identification of novel treatment strategies for neurodegenerative diseases.
Worm models of Parkinson's disease that expressed either a mutated LRRK2 gene or a mutated alpha-synuclein gene--both of which cause Parkinson's--were crossed with a long-lived strain of the worm to create two new strains with longer lifespans.
Van Raamsdonk's team then compared the two original LRRK2 and alpha-synuclein models with normal lifespans to the resulting two long-lived Parkinson's models, and found that long-lived LRRK2 and alpha-synuclein worms lost dopamine neurons at a much slower rate than their counterparts with normal lifespans. In fact, the long-lived LRRK2 worms had more dopamine neurons left on day 30 of the study than the LRRK2 worms with a normal lifespan of three weeks had on day eight of adulthood. Slowing aging also effectively reduced motor deficits related to the loss of dopamine-producing cells and eliminated the increased sensitivity to stress shown by worms with a normal lifespan.

From worms to people

The long-lived strain of C. elegans Van Raamsdonk used for the crosses has a mutation in daf-2, a gene that encodes for a member of the insulin and IGF1 signaling pathways. Genes in these pathways are also associated with longevity in humans; however, therapies that affect the pathways may need to be carefully controlled to mitigate potential side effects. As such, Van Raamsdonk plans to investigate this link in other Parkinson's disease models and to search for additional pathways involved in longevity that have a lower risk of side effects, while still effectively slowing or preventing disease onset.
Adapted by MNT from original media release

New research by biologists at the University of York could lead to improved methods of detection for early-onset Parkinson's disease.

Fruit flies

Nov.25, 2015

New research by biologists at the University of York could lead to improved methods of detection for early-onset Parkinson's Disease (PD).
Recording the responses of fruit flies (Drosophila melanogaster) to different visual patterns, using methods adapted from the study of vision in humans, scientists in York's Department of Biology investigated the nervous systems of flies with different types of Parkinson's mutations.
Funded by the Wellcome Trust, researchers compared flies carrying mutations associated with early-onset Parkinson's with 'normal' control flies, and found increased neuronal activity to stimulation in the former group in 'young' flies.
By mapping the visual responses of fruit flies with different Parkinson's genes, the scientists built a substantial data bank of results. Using this they were able to classify unknown flies as having a Parkinson's related mutation with 85 per cent accuracy.
Researchers believe it may be possible to transfer this method back to the clinic where early changes in vision may provide a 'biomarker' allowing screening for Parkinson's before the onset of traditional motor-symptoms. Therefore, profiling human visual responses could prove an accurate and reliable test in diagnosing people with early-onset PD.
This method is also likely to succeed when transferred to human detection of Parkinson's, as visual profiling in humans has proved accurate in the past in detecting genetic markers. In this study, as more complex light stimulations have been used, a more accurate picture of detecting a wider variety of different genetic markers has been revealed.
Dr Ryan West, Postdoctoral Research Scientist in York's Department of Biology and Lead Author on the study, said: "Increased visual activity in young fruit flies with early-onset Parkinson's mutations is a significant finding, as it may provide an early-onset biomarker for people at risk of Parkinson's.
"Using 64 different combinations of visual stimuli, we now have a comprehensive bank of the reactions of fruit flies carrying different genetic mutations. We can see that fruit flies carrying different mutations have distinct patterns of visual responses, suggesting this is a reliable method in classifying Parkinson's genotypes.
"We hope this method may be translatable to the clinic where changes in vision may provide an early indication of early-onset Parkinson's. Such early detection is essential if we are to understand disease progression and develop novel therapeutics."

Tuesday, November 24, 2015

Ask the MD: Glutathione and Parkinson’s

Posted by  Rachel Dolhun, MD, November 24, 2015
In this post I’m discussing a substance you may have heard of — glutathione. It’s made naturally by the body but is also available in certain foods and over-the-counter supplements. Glutathione levels decrease with aging and certain conditions, including Parkinson’s disease (PD). In people with PD, glutathione levels are lower in the brain, specifically in the substantia nigra (the area in which dopamine cells are lost). Also, the level of reduction in glutathione has been associated with Parkinson’s disease severity (less glutathione, more advanced PD).  
The Role of Glutathione
Glutathione functions as an antioxidant — a compound that clears out free radicals. Free radicals are molecules that are potentially toxic to cells. They are formed in the body from normal metabolism (such as converting food to energy), but are increased by exposure to environmental toxins, such as cigarette smoke and air pollution. Buildup of free radicals contributes to a condition called oxidative stress, which is associated with aging and PD. Antioxidants may therefore offset oxidative stress by removing free radicals.
In addition to its work as an antioxidant, glutathione may support the mitochondria — the cell’s energy producers. This could prevent cell death, meaning that glutathione could conceivably operate as a “neuroprotective” agent — one that could slow or stop the progression of PD.
The Research on Glutathione 
For these reasons, glutathione supplementation has been and is currently being studied to determine if it could provide symptomatic benefit to people with Parkinson’s. Glutathione can be given through several routes — oral, intravenous (IV) and intranasal (through the nose). Each method has advantages and limitations.
Although a pill would be ideal, oral glutathione is poorly absorbed from the digestive system and doesn’t get into the brain very well.  
Intravenous administration avoids these absorption concerns and raises blood levels of glutathione. Two clinical trials of IV glutathione have been conducted. The first (reported in 1996) was open-label — all nine people with Parkinson’s were aware they were given IV glutathione. Participants’ motor symptoms improved, and this benefit lasted for two to four months following discontinuation of glutathione. The second study (reported in 2009) was a randomized-controlled trial of 20 people with PD — half were given placebo and half were treated with IV glutathione. The therapy was shown to be safe, well tolerated and possibly beneficial for symptoms. To determine if IV glutathione is a truly efficacious symptomatic therapy for Parkinson’s, larger, randomized, placebo-controlled trials need to be done. These haven’t been performed, though, perhaps because of this treatment’s downsides — IV glutathione can be expensive, inconvenient and associated with potential side effects (bleeding, infection, blood clots). There are also other ways to give glutathione (intranasally) that are less invasive and may be more effective.
Early research efforts toward intranasal glutathione showed that it is safe, well tolerated and raises levels of glutathione in the brain (as seen on imaging scans). An MJFF-funded Phase IIb placebo-controlled trial is currently examining the effects of intranasal glutathione on Parkinson’s motor symptoms. If these results are positive, a Phase III trial will aim to determine whether intranasal glutathione is disease-modifying.
The Current State of Glutathione
Since glutathione is categorized as a supplement, it doesn’t require U.S. Food and Drug Administration approval, and is already widely available. Even though it isn’t very effective, oral glutathione is offered by many retailers. Some intranasal sprays (different formulations from those being used in studies) are sold as well. And even though there is no standard dosing protocol and insurance often doesn’t cover the cost, many doctors and clinics will administer intravenous glutathione.
So why not add it to your regimen? While glutathione is a promising therapy for Parkinson’s, the benefit and efficacy have yet to be confirmed.
The Bottom Line
The desire and need for better symptomatic therapies and certainly for a disease-modifying treatment for those living with PD is more than understandable. We sense that urgency and are working to move promising therapies through the pipeline and to patients as quickly as possible.
Until these are proven, however, proceed with caution. Any therapy — whether it’s a supplement, an over-the-counter medication, or even if it’s described as “all natural” — can cause side effects and could interact with prescription drugs. Discuss all therapies with your doctor before taking them. Weigh the pros and cons, and always check the background and credentials of the physician and pharmacy providing the therapy.
The “Ask the MD” series is supported by Acorda Therapeutics. While our generous sponsors make the “Ask the MD” program possible, their support does not influence MJFF’s content or perspective.

Parkinson Disease-Spotlight on Treatment Advances Webinar/Teleconference, January 26, 2016 launched by the American Parkinson Disease Association

November 30, 2015 (PRWEB) November 24, 2015 -- 

Understanding treatment options to provide the best quality of life for those living with Parkinson’s  New York, NY –
The American Parkinson Disease Association (APDA) is pleased to announce a new Webinar/Teleconference program, “Parkinson Disease-Spotlight on Treatment Advances” on Tuesday, January 26, 2016 (12:00PM–1:00PM ET; 11:00AM–12:00PM CT; 10:00AM–11:00AM MT; 9:00AM–10:00AM PT). This program, funded by AbbVie, will provide an expert perspective on the latest treatment advances for Parkinson’s disease. 
“The importance of timely information cannot be overvalued when you are living day to day with a chronic disease”, said Leslie A. Chambers, President & CEO of APDA. “Many Parkinson’s patients do not see their clinicians on a regular basis, and frequently only when they have symptom management problems. This teleconference will provide a scan of the current treatment options for Parkinson’s disease patients, newly released products and a brief review of potential promising therapies in the pipeline.”
David G. Standaert, MD, PhD, Chairman of APDA’s Scientific Advisory Board and John N. Whitaker Professor and Chair of Neurology at The University of Alabama Birmingham School of Medicine will present this program designed to provide people with Parkinson’s, care partners, family members, and healthcare providers an important overview of the options available today. 
Click here to register online. To register by phone, please call toll-free (800) 223-2732.
A confirmation including program details will be sent upon registering for the program.
American Parkinson Disease Association 

The American Parkinson Disease Association (APDA) was founded in 1961 with the dual purpose to Ease the Burden - Find the Cure for Parkinson's disease. In that time, APDA has raised and invested more than $87 million to fund research, patient services and education, and elevate public awareness. As the country's largest Parkinson's grassroots organization, APDA aims to Ease the Burden for the more than one million Americans with Parkinson's disease and their families through a nationwide network of Chapters, Information and Referral (I&R) Centers, and support groups. APDA pursues its efforts to Find the Cure by funding Centers for Advanced Research and awarding grants to fund the most promising research toward discovering the cause(s) and finding the cure for Parkinson's disease.


AbbVie, is a global, researched-based biopharmaceutical company, is committed to ongoing Parkinson's education to raise awareness about the condition, and research to improve the lives of those living with and impacted by this disease. 
Stephanie Paul | APDA Vice President Marketing & Development | 718-981-8062 | spaul(at)apdaparkinson(dot)org

For the original version on PRWeb visit:

Infertile worms resist infection-induced neurodegeneration

Nov. 24, 2015

Duke researchers have shown that infection with pathogenic bacteria causes neurodegeneration in the worm C. elegans. Infected animals displayed neural changes that are hallmarks of neurodegeneration in patients with illnesses like Alzheimer’s disease. The green region in this worm is a wavy, branched and beaded neuron, indicating neurodegeneration. Photo credit: Alejandro Aballay lab

Intriguing exception to pattern of infection leading to neuro-disease.

The connections are still obscure, but mounting evidence points to a link between infections, the immune system, and neurodegenerative diseases like Alzheimer's, ALS, and Parkinson's.
Now, a team of Duke University researchers has shown that infection with live, pathogenic bacteria causes neurodegeneration in the worm C. elegans. Infected worms display a number of changes that are hallmarks of neurodegeneration in aging humans and patients with illnesses such as Alzheimer's disease.
The study, which appears online now and in print December 4, 2015 in the Journal of Biological Chemistry, also yielded a big surprise: infertile animals appear to be protected from neurodegeneration.
"In worms, there may be some type of signal from the sex cells or germline that plays a role in infection-induced neurodegeneration," said Alejandro Aballay, Ph.D., senior study author and associate professor of molecular genetics and microbiology at Duke University School of Medicine.
"That was definitely unexpected, though we know that infertility liberates energy that would have been spent on producing the germline and directs it toward tissue repair and other maintenance," Aballay said. "It will be interesting to figure out how the response to pathogens fits into this scheme."
In recent years, researchers have begun to notice a problematic relationship between pathogens and neurodegeneration. Multiple studies have shown that patients living with chronic infections are particularly susceptible to neurodegenerative diseases. What appears to happen is microbes infect a patient, alerting the immune system and unleashing inflammation, which progressively destroys neurons. This unintended side effect does not benefit the microorganism, and it certainly doesn't benefit the host.
Because it is so difficult to study this process in humans, Aballay's lab turned to the nematode worm, C. elegans, as a model. This 1-millimeter, transparent worm has a much simpler nervous system, consisting of only 302 neurons that represent most types of neurons in the mammalian brain. It also has a rudimentary immune system.
In the laboratory, these worms typically inhabit Petri dishes covered in a lawn of E. coli bacteria, which the animals graze all day. To infect the worms, Aballay and his colleagues simply replaced the worm's typical chow with the common bacterial pathogen Pseudomonas aeruginosa. They also tagged the animals' neurons with a fluorescent label so the researchers could visualize any neurodegenerative changes associated with infection.

TThe researchers witnessed a number of neural changes that are hallmarks of neurodegeneration. For example, they saw beaded neurons, nerve cells with little round outgrowths that give the appearance of beads. They also found areas where the neurons, which are normally straight like an arrow, were branched or wavy.
"Neurons are designed to act like a straightforward superhighway that sends signals from one cell to another," said Aballay. "These wavy neurons are more like a mountain route, where things go very slow and inefficiently because it turns and curves."
In humans, these changes would be accompanied by behavioral defects, perhaps making it harder to remember a name or where you put the car keys. In worms, the researchers found that these neural changes also had functional consequences. Normally, the animals would be able to sense and move toward their favorite treat -- salt -- but when their neurons were affected, so was their ability to respond to the stimulus.
Next, the researchers wanted to determine if there were any genes that could protect against infection and neurodegeneration in worms. They mutated hundreds of worms, infected them with the same pathogen as before, and then looked to see if any were resistant to infection-induced neurodegeneration. The researchers found one particularly promising candidate, which contained a mutation in a gene called mes-1. Interestingly, all the worms with this mutation lacked the sex cells needed to produce offspring.
In additional genetic studies, Aballay and his colleagues found that another gene called DAF-16 was required for resistance to neurodegeneration in these mutant animals. Its human equivalent, a gene called FOXO6, is known to function at the intersection of pathways controlling immunity, longevity and stress responses.
"In the future, we plan to focus more on what is happening at the level of the neuron, to understand how the neuron senses pathogenic molecules or inflammatory cues, and how sensing those cues ultimately triggers neurodegeneration," said Aballay.
Adapted by MNT from original media release