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Wednesday, February 1, 2017

A fifth of dementia cases may be caused by air pollution, study suggests

February 1, 2017

Researchers found that older women exposed to high levels of fine particle air pollution were much more likely to develop dementia.


New research strengthens the previously reported link between air pollution and cognitive decline, after finding that exposure to fine particulate matter could significantly raise the risk of developing Alzheimer's disease and other dementias.

The research found that exposure to high levels of particulate matter 2.5 (PM2.5) - tiny air pollution particles that are up to 2.5 micrometers in diameter - increased older women's risk of dementia by over 90 percent, compared with low PM2.5 exposure.
Senior study author Prof. Caleb Finch, of the Leonard Davis School of Gerontology at the University of Southern California (USC), and colleagues say that if their findings apply to the general population, then PM2.5 could account for around a fifth of dementia cases.
The researchers recently reported their findings in the journal Translational Psychiatry.
PM2.5 are fine particles consisting of solids and liquid droplets that are emitted from sources involving combustion, such as power plants and motor vehicles.
PM2.5 are 2.5 micrometers in diameter or smaller. To put their size into perspective, the diameter of a PM2.5 particle is around 30 times smaller than that of a human hair. 
Because they are so small, PM2.5 are easily inhaled, which can pose numerous problems for health. According to the United States Environmental Protection Agency (EPA), exposure to fine air particles can increase the risk of heart attacksasthma, and reduced lung function, as well as premature death for individuals with heart or lung disease.
In recent years, studies have suggested that exposure to such pollution may also raise the risk of dementia.
Prof. Finch and team decided to investigate this association further in their new study.

Alzheimer's risk increased by 92 percent with high PM2.5 exposure

The researchers arrived at their findings by analyzing the data of 3,647 women from 48 U.S. states who were part of the Women's Health Initiative Memory Study (WHIMS). 
All women were aged between 65 and 79 and were free of dementia upon study enrollment. As part of the WHIMS, participants' cognitive function was assessed annually.
Using data from the EPA, the team estimated the women's daily PM2.5 exposure at their place of residence.
Compared with women who lived in areas exposed to low PM2.5 levels, those who resided in areas with high PM2.5 levels - defined as levels that that exceeded the EPA's permissible limit in 2012 (35 micrograms per cubic meter of air) - were found to be at an 81 percent greater risk of global cognitive decline and have a 92 percent increased risk of developing Alzheimer's disease and other dementias.
The results remained after accounting for numerous confounding factors, including race and ethnicity, socioeconomic status, lifestyle, and the presence of other medical conditions.
The researchers estimated that if their findings ring true among the general population, then exposure to high PM2.5 levels could contribute to approximately 21 percent of dementia cases.

Air pollution may worsen plaque formation in presence of APOE ε4 gene

Interestingly, the increased risks of global cognitive decline and dementia as a result of high PM2.5 exposure were strongest among women who possessed the APOE ε4 gene, which is associated with the development of Alzheimer's.
With this in mind, the team conducted mouse experiments in order to investigate how PM2.5 exposure affects the brain in the presence of APOE ε4.
Using cutting-edge particle concentrators, the researchers exposed two groups of female mice to nano-sized air pollution for 15 weeks. One group possessed the APOE ε4 gene and one did not.
Study co-author Constantinos Sioutas, of the USC Viterbi School of Engineering, explains that the particle concentrators "essentially take the air of a typical urban area and convert it to the air of a freeway or a heavily polluted city like Beijing."
"We then use these samples to test exposure and assess adverse neurodevelopmental or neurodegenerative health effects," he adds.
Compared with mice without the APOE ε4 gene, those that possessed the gene were found to accumulate around 60 percent more beta-amyloid plaque in their brains. Plaques are clusters of beta-amyloid protein, which are believed to destroy neurons.
According to the researchers, their findings provide "clear evidence" that fine particle air pollution is related to dementia risk, and they provide the first evidence that exposure to these particles can exacerbate beta-amyloid accumulation. 
The authors add:
"Moreover, these joint data from humans and mice provide the first evidence that neurodegenerative effects of airborne PM may involve gene-environment interactions with APOE4, the major genetic risk factor for pathological brain aging and AD [Alzheimer's disease]. 
The association between PM2.5 exposure and increased dementia risk suggests that the global burden of disease attributable to PM2.5 pollution has been underestimated, especially in regions with large populations exposed to high ambient PM2.5."
The team plans to conduct further studies that will assess how high PM2.5 exposure influences cognitive function in both men and women.

http://www.medicalnewstoday.com/articles/315605.php

B.C. Parkinson’s patients want funding for expensive drug to improve quality of life

February 1, 2017

A drug called Duodopa can be a life-changer for people with Parkinson’s disease. The problem is, it’s so expensive few patients in B.C. have access to it. As Nadia Stewart reports, Parkinson’s patients don’t understand why their government is leaving them to suffer.

Video:


Another B.C. family is lending their voice to the growing number of calls for the province to reconsider it’s decision not to cover a treatment for some living with Parkinson’s Disease.
Barry Mansfield is one of about a dozen people in the province who aren’t responding to traditional treatments. Mansfield says he takes upwards of 60 pills a day, but they aren’t effective anymore.
Mansfield, who was once a paragliding, tennis playing, sailing, retired teacher from Hope, is now sometimes housebound, never knowing how his body will respond on any given day.
“If you said to me we’re gonna have lunch tomorrow at 6, I might not be ready until 10. I might not be ready for two days,” Mansfield said.
Barry Mansfield in his earlier days before getting Parkinson\’s Disease.


His doctor has told him he needs a drug called Duodopa. The patient needs to be hooked up to an insulin-pump-type machine and the drug would deliver a steady dose of levodopa and carbidopa into the person’s gut. While he likely won’t be returning to the healthy active lifestyle he once had, they believe the drug could significantly improve his mobility and quality of life.
Health Canada has approved the drug but B.C. won’t cover the cost of it, citing a 2009 report from the Common Drug Review (CDR), which recommended the drug not be covered by participating PharmaCare programs. Among the two key reasons listed, Eric Lun, executive director of B.C.’s Drug Intelligence and Optimization Branch, has said cost is a key factor.
“At the manufacturer’s list price of $166/day, the annual cost of therapy with Duodopa is over $60,000 per patient per year, compared with $3 per day or approximately $1,095 for the oral forms of the same drug,” Lun wrote in a December 13, 2016 email.
“This represents a 5,379 per cent increase in the price of levodopa carbidopa from the oral form to the Duodopa form of the drug.”
Concerns were also raised about the quality of the two evaluated trials presented by the drug’s manufacturer, AbbVie.
Citing the Canadian Expert Drug Advisory Committee, Lun said the trials were “open label, of small size, had high proportions of withdrawals, and were in patient populations that did not represent those most likely to use Duodopa.”
AbbVie says it has done more research and new evidence points to the drug’s effectiveness. They also say Ontario, Manitoba, Quebec, Alberta and the Yukon cover the drug on a case-by-case basis; which frustrates Mansfield’s daughter Juli Oldham.
“There’s probably about 10 or 12 people in the province right now that could really benefit from this treatment that’s not available in B.C…. not covered currently by Pharmacare and it’s devastating. It’s scary,” Oldham said.
The province maintains that if AbbVie resubmits Duodopa for the Common Drug Review process, they will look at the new evidence and make a decision from there. Abbvie has not resubmitted for a review, saying it would rather work directly with each individual province.
AbbVie said they are “concerned about re-submitting to the Common Drug Review (CDR) as it could negatively affect the existing coverage in jurisdictions that have approved funding without a CDR resubmission.”
According to the Parkinson’s Society B.C., 13,000 people in the province live with the condition. Jean Blake, CEO of Parkinson’s Society BC, is hoping the province will look beyond the bureaucratic process and consider the day-to-day pain patients are in.
“It’s really heartbreaking to hear some of the stories when we know that the therapy is within reach,” she said.
Mansfield and his family remain hopeful the B.C. government will have a change of heart. His daughter says the family is running out of time and options.
“It’s horrifying to think that there’s something that would change his life for the better and we can’t provide that for him. It’s a desperate feeling.”
http://globalnews.ca/news/3220534/b-c-parkinsons-patients-want-funding-for-expensive-drug-to-improve-quality-of-life/

Targeting Parkinson's-linked protein could neutralize two of the disease's causes

February 1, 2017

Dopamine-making cells in a mouse brain. Credit: Sung-ung Kang/Johns Hopkins Medicine


Researchers report they have discovered how two problem proteins known to cause Parkinson's disease are chemically linked, suggesting that someday, both could be neutralized by a single drug designed to target the link. A report on their discovery appears in the Jan. 24 issue of Cell Reports.The investigators' new experiments build on evidence reported in 2011 that reducing the amount of a protein called PARIS in mice with the rodent equivalent of Parkinson's disease protects against the loss of dopamine-making neurons.

Since then, according to Ted Dawson, M.D., Ph.D., professor of neurology and director of the Institute for Cell Engineering at the Johns Hopkins University School of Medicine, the research team suspected PARIS was linked chemically to other important Parkinson's proteins. "In this study, we were able to confirm that suspicion," he says.
Dawson explains that a hallmark of Parkinson's disease is the death of brain cells that produce the signaling molecule, or neurotransmitter, dopamine. Dopamine depletion, in turn, causes the classic symptoms of Parkinson's disease, such as tremors, muscle stiffness and lack of muscle coordination. Mutations in the gene for a protein called Parkin are known to cause the death of dopamine neurons; less commonly, defects in another protein, PINK1, can have the same effect.
In mouse experiments done in collaboration with researchers at Mayo Clinic in Florida, Dawson's team investigated whether both proteins might act through a single intermediary: PARIS.
In their 2011 study, Dawson and his collaborators had used mice and human brain tissue to find that Parkin adds a chemical tag known as ubiquitin to PARIS that signals other proteins to break it down.
To find out whether PINK1 and PARIS have a similar relationship, the researchers ran biochemical tests on purified proteins that revealed that PINK1 and PARIS interact. Dawson says the results revealed that while PINK1's normal role is to add a chemical tag known as a phosphate group to a certain spot on the PARIS protein, defective forms of PINK1 linked to Parkinson's disease cannot add that tag.
The phosphate addition, he says, kicks off a chain of events that ultimately leads to the dismantling of the PARIS protein, Dawson says, a cause-and-effect relationship his team verified by reducing the amount of PINK1 in lab-grown human cells, which led to a threefold increase in the amount of PARIS. Similarly, reducing the amount of PINK1 made in living mice by more than 80 percent led to a doubling in the amount of PARIS present.
In another experiment, the research team ramped up PINK1 production in lab-grown human cells and found that the resulting increase in cell death was alleviated if PARIS levels also increased. But if PINK1 was tweaked to eliminate the sites where PARIS normally adds a phosphate group, PARIS was unable to rescue the cells.
Since both Parkin and PINK1 protect  by causing PARIS' breakdown, Dawson suggests that defects in either could be remedied if a treatment can be found that hobbles PARIS. "Mutations in the genes for both Parkin and PINK1 have now been linked to Parkinson's disease," he says. "Parkin is a particularly big player that seems to be at fault in many inherited cases; it's also inactivated in sporadic cases of the disease. So a drug targeting PARIS could potentially help many patients."
More than 1 million people in the United States live with Parkinson's disease. The disease gradually strips away motor abilities, leaving people with a slow and awkward gait, rigid limbs, tremors, shuffling and a lack of balance. Its causes are not well-understood. Currently available treatments, such as medications and deep brain stimulation, can alleviate symptoms but do not cure it or slow its progression.
Dawson emphasizes that clinical application of their discovery must await not only further studies in animals, but also years of drug design and clinical research. But he says their discovery has the potential to simplify and focus the development of better treatments.
Other authors on the paper are Yunjong Lee, Daniel A. Stevens, Sung-Ung Kang, Haisong Jiang, Yun-Il Lee, Han Seok Ko, Leslie A. Scarffe, George E. Umanah, Hojin Kang, Sangwoo Ham, Tae-In Kam, Kathleen Allen, Saurav Brahmachari, Jungwoo Wren Kim, Stewart Neifert, Seung Pil Yun, Valina L. Dawson and Joo-Ho Shin, all of the Johns Hopkins University School of Medicine, and Fabienne C. Fiesel and Wolfdieter Springer of Mayo Clinic.
More information: Yunjong Lee et al, PINK1 Primes Parkin-Mediated Ubiquitination of PARIS in Dopaminergic Neuronal Survival, Cell Reports (2017).  DOI: 10.1016/j.celrep.2016.12.090 
Journal reference: Cell Report
https://medicalxpress.com/news/2017-02-parkinson-linked-protein-neutralize-disease.html

Hand Grip Test May Indicate Decline in Physical Functions For Parkinson’s Patients

NEUROSCIENCE NEWS
Summary: Handgrip test appears to be one of the most reliable measures of physical function decline in Parkinson’s patients.


Source: UBC Okanagan campus.

The participants wore a portable monitoring device to measure muscle activity with the device recording electrical activity of muscles in the arms and legs for approximately eight hours. NeuroscienceNews.com image is for illustrative purposes only.


UBC researchers Jenn Jakobi and Gareth Jones, both Health and Exercise Sciences professors at UBC’s Okanagan campus, recently completed a study that examined the methods used to monitor the progressive advancement of Parkinson’s disease (PD)–a degenerative disease that affects the central nervous system.

The study compared results from electromyography assessments of leg and arm muscles to basic physical performance tests such as gait speed, balance and hand-grip strength. The results were surprising.

“It became very clear that the hand-grip test was one of the functional tests that proved to be a reliable and valuable test measure,” says Jakobi. “The hand-grip test is an easy and conclusive way to test muscle strength decline in this group of people.”

The study involved 23 men and women with PD and 14 people without the disease, all 50 years or older living independently in Kelowna. The participants wore a portable monitoring device to measure muscle activity with the device recording electrical activity of muscles in the arms and legs for approximately eight hours. Participants also underwent three physical function tests–hand-grip, gait and balance–each morning and afternoon.

Jones says the data gleaned from the three physical tests was as conclusive and as informative as the lengthy recordings of muscle activity. And the tests were easier for participants and those administering the experiments.

“The hand-grip dynamometer is a tool that is easily accessible, easy to use, and is reliable,” says Jones. “In addition they are readily available to health professionals such as family doctors, community therapists and physiotherapists.”

“It seems these devices have come full circle and are back being used by clinicians,” adds Jakobi. “It’s a tool that is ideal for Parkinson’s patients as you can easily record a decline in an individual’s physical strength and function as the disease progresses.”

Patients with PD suffer symptoms like uncontrollable shaking, slowness of movement, and eventually difficulty with balance, coordination and walking. It’s important for health care professionals to track early functional decline of Parkinson’s patients, says Jakobi. In this way, individual health can be monitored and future falls related to the disease prevented.

According to Statistics Canada more than 67,000 Canadians are living with Parkinson’s today, and it is mostly diagnosed in men over the age of 45.
The study was recently published in the journal Archives of Physical Medicine and Rehabilitation.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: Funding provided by Canadian Institutes of Health Research, Institute of Neurosciences, Mental Health and Addiction, Parkinson Society Canada.
Source: Patty Wellborn –  UBC Okanagan Campus 
Image Source: NeuroscienceNews.com image in the public domain.
Original Research: Abstract for “Handgrip Strength Related to Long-Term Electromyography: Application for Assessing Functional Decline in Parkinson Disease” by Gareth R. Jones, Kaitlyn P. Roland, Noelannah A. Neubauer, and Jennifer M. Jakobi in Archives of Physical Medicine and Rehabilitation. Published online November 5 2016 doi:10.1016/j.apmr.2016.09.133


Abstract

Handgrip Strength Related to Long-Term Electromyography: Application for Assessing Functional Decline in Parkinson Disease
Objective
To determine which clinical measures of physical function (ie, gait, balance, and grip strength) best represent long-term electromyography in persons with Parkinson disease (PD) compared with those without PD.

Design
Cross-sectional study.

Setting
Local community.

Participants
A sample (N=37) of men and women with PD (n=23) and those without PD (n=14), living independently at home, older than 50 years of age, from the local community.

Interventions
Not applicable.

Main Outcome Measures
Measures of gait, balance, and grip strength were completed, and electromyography was examined in biceps brachii, triceps brachii, vastus lateralis, and biceps femoris during a 6.5-hour day. Muscle activity was quantified through burst in electromyography (>2% of the normalized maximum voluntary exertion with a continuous activity period of >0.1s). Stepwise multiple regression models were used to determine the proportion of variance in burst characteristics explained by clinical measures of physical function in PD.

Results
Grip strength was the best predictor of muscle activity in persons with PD (R2=.17–.33; P<.04), whereas gait characteristics explained muscle activity in healthy controls (R2=.40–.82; P<.04).

Conclusions
Grip strength could serve as an effective clinical assessment tool to determine changes in muscle activity, which is a precursor to functional loss in persons with PD.

“Handgrip Strength Related to Long-Term Electromyography: Application for Assessing Functional Decline in Parkinson Disease” by Gareth R. Jones, Kaitlyn P. Roland, Noelannah A. Neubauer, and Jennifer M. Jakobi in Archives of Physical Medicine and Rehabilitation. Published online November 5 2016 doi:10.1016/j.apmr.2016.09.133

Tuesday, January 31, 2017

Could the link between gut bacteria and the brain help treat disorders like anxiety and depression?

January 31, 2017


Neuroscientists are only starting to study the links between gut bacteria and the brain, writes Jamie Ball, and it may change how we treat disorders like anxiety and depression



For those of you who assumed the reasoning behind "gut instinct" or "going with your gut" or "feeling gutted" or "butterflies in your tummy" to be groundless old wives' tales, science is asking you to think again.

Mounting evidence over the last decade suggests that gut microbes help shape normal neural development and brain biochemistry. And while the science continues to unfold the mysteries of how and why the microbiota-brain axis so deeply influences our mood and behaviour, it is hoped research will reveal innovative, diet-based treatments not just for depression and anxiety, but for the likes of Parkinson's, Alzheimer's, autism and schizophrenia too.
The intestine and the brain are closely connected through the bidirectional communication of the brain-gut axis, which comprises of interactions with intestinal microbiota, or gut bacteria. These release immune-activating molecules that have the potential to play a crucial part in brain regulation, impacting upon our mood, thoughts and behaviour.
"It will remain that the heart is our emotional centre for love and romance," says Professor Jane Foster of the Department of Psychiatry and Behavioural Neurosciences at McMaster University in Ontario, Canada.
"However, there is a place for gut feelings in understanding the biological pathways that influence mood and mental health, which are, in fact, quite distinct. Neuroscientists and others are only just starting to study the ways that microbiota influence the brain."
Foster says the latest research demonstrates a central role for gut microbiota in our normal healthy metabolism, as studies show that disruption or alterations in the profile of gut microbiota can increase the risk of metabolic disorders, such as obesity and diabetes.
"Recent work studying communication between the brain and the gut have also identified a functional link between gut microbiota and brain function, with particular attention to depression and anxiety," adds Foster.
Enter probiotics. Defined simply as "microorganisms that are believed to provide health benefits when consumed", probiotics have only entered the general consumer's radar over the last quarter century, most typically in association with certain yoghurts. But the research behind probiotics dates back over a century. In 1907, Nobel laureate, Élie Metchnikoff, had originally suggested that intestinal microbes' dependence on diet allows us to replace harmful microbes with useful ones.
However, the numerous beneficial claims made about using commercial probiotics are not always backed up by scientific evidence. And while most conclusive scientific research on this topic to date has been carried out on rodents, two separate studies in recent years provide greater hope.
A 2013 study by the Oppenheimer Family Centre for Neurobiology of Stress at the Department of Medicine in UCLA, California, established that the consumption of a fermented milk product with a yoghurt-based probiotic for four weeks by healthy women affected activity of brain regions that "control central processing of emotion and sensation".
Furthermore, a 2015 triple-blind assessment by scientists at the Netherlands' Leiden University's Institute for Psychological Research, used a multi-species probiotic food supplement on 20 healthy adults over four weeks. The results provided the "first evidence that the intake of probiotics may help reduce negative thoughts associated with sad mood. Probiotics supplementation warrants further research, as a potential preventive strategy for depression".
Which is where probiotics enters the field of psychobiotics; a live microorganism, which when administered in adequate amounts, confers a health benefit in patients suffering from psychiatric illness.
"While much of the early work suggesting the microbiota influence brain function and behaviour came from animal studies," says Foster, "evidence is accumulating from studies in healthy individuals and in clinical populations that probiotics reduce depressive and anxiety-related symptoms, but also reduce the body's physiological response to stress, where individuals receiving probiotics have lower levels of circulating stress hormones."
It appears there is massive microbiome potential this century for the prevention or treatment of certain brain-related illnesses. One case in point is Parkinson's disease: the gut microbes of those suffering from Parkinson's have been found to be radically different to non-sufferers. However, whether such degenerative diseases can be effectively treated by altering the gut microbe composition remains to be seen. In addition, it is still too early to tell whether psychobiotics could, in time, come to replace conventional anti-depressants, but it's arguably neuroscience's key challenge for the next decade.
"Our bacteria development early in life is needed for early brain development, and perhaps an imbalance might be a predisposing factor for a number of brain disorders," says Professor John Cryan in his 2015 TEDMED talk. A neuropharmacologist and microbiome expert from University College Cork, Cryan has published over 190 peer-reviewed articles and book chapters.
"In the 20th century we focused on killing microbes with antibiotics - that was the major focus. Over the last number of years we have really appreciated that microbes have so much benefit and that their power can be harnessed in both health and disease.
"So perhaps the secret to our own happiness may not lie in the self-help section of the local bookstore, but maybe within your microbiome, and that your state of mind might be dependent on your state of gut."

Good gut, bad gut

Microbes can be found in many parts of our bodies, such as our skin and lungs, where they play an important role in host-environment interactions. But we have way more bacteria in our intestines than we do cells in our body, and therefore gut microbes capture the most attention.
These are critical to the healthy development of our immune system and our brains, as "good" gut bacteria helps us digest complex polysaccharides in our diet, which play a critical role in the normal development of the immune system.
It's also been discovered that the industrialisation of developed nations over the last couple of centuries has wiped out some of the diversity and richness of microbes that our descendants would have shared, as emulsifiers and sweeteners, for example, as well as processed food, have done little to help our microbe composition.
However, a tenable link between the consumption of such foods and the onset of mental illnesses, or brain-related degenerative diseases, has yet to be established, but we are likely to know a lot more over the next five to 10 years about how water-tight and verifiable any such link may be.
According to Professor Jane Foster of McMaster University in Ontario, the composition of our microbiota is influenced by both our own genetics and by the environment (diet, stress, exercise, antibiotics and other medications) and by other important factors (age and gender).
"We are not able to change our own genetics but we may be able to influence it through other choices, such as how gene-environment interactions influence our microbiota and our health.
"From my perspective the most important threat to the gut microbiota, with respect to mental health, is early life environment including diet, stress and medications. These influence microbiota but also influence brain wiring and may influence risk of disease later in life."
According to Foster, antibiotics definitely reduce the diversity and composition of the microbiota, but she is cautious about overstating the perceived damage.
"Following a short course of antibiotics, our gut microbiota return to normal. It is likely that chronic or repeated exposure to antibiotics would be associated with more permanent damage to the system. In fact, in some situations, a short course of antibiotics has a mood-elevating effect. This might relate to the reduced inflammation or the anti-inflammatory effects of this type of medication."

http://www.independent.ie/life/health-wellbeing/health-features/could-the-link-between-gut-bacteria-and-the-brain-help-treat-disorders-like-anxiety-and-depression-35403494.html

Brody: Exercise, early and often, counters Parkinson's

January 31, 2017


Susan Sills, a Brooklyn artist who until recently made life-size cutouts on plywood using a power saw, long suspected she might be at risk for developing Parkinson's disease. Both her mother and grandfather had this neurological movement disorder, and she knew that it sometimes runs in families.
So she was not surprised when at age 72 she first noticed hand tremors and a neurologist confirmed that she had the disease. But to watch her in action three years later, it would be hard for a layperson to tell. She stands straight, walks briskly, speaks in clarion tones and maintains a schedule that could tire someone half her age.
Having wisely put the power saw aside, Sills now makes intricately designed art jewelry. She is also a docent at the Brooklyn Museum, participates in a cooperative art gallery and assists her husband's business by entertaining customers.
Sills attributes her energy and well-being partly to the medication she takes but primarily to the hours she spends working out with a physical therapist and personal trainer, who have helped her develop an exercise regimen that can alleviate Parkinson's symptoms and slow progression of the disease.
"The exercises opened me up," said Sills, allowing such symptoms as small steps, slow movements and tiny, cramped handwriting to subside.
"The earlier people begin exercising after a Parkinson's diagnosis, and the higher the intensity of exercise they achieve, the better they are," Marilyn Moffat, a physical therapist on the faculty of New York University, said. "Many different activities have been shown to be beneficial, including cycling, boxing, dancing and walking forward and backward on a treadmill. If someone doesn't like one activity, there are others that can have equally good results."
Unfortunately, Moffat added, "no one tells people with Parkinson's what they could and should be doing unless they get to a physical therapist." The typical delay in starting an effective exercise program also stems from the ability of medication to alleviate early symptoms, leaving patients with little incentive to exercise.
While everyone can benefit from exercise, it is especially important for people with a progressive movement disorder like Parkinson's that can result in weakness, stiffness, difficulty walking, poor balance and falls, as well as impaired cognitive processing. Regular exercise bestows increased levels of fitness, a greater sense of well-being, stronger muscles and bones, healthier joints, more efficient breathing, and better digestion and blood circulation. The result is enhanced physical, mental and cognitive health, all of which are especially important to people with a chronic ailment.
For Parkinson's patients in particular, regular exercise tailored to their needs can result in better posture, less stiffness, improved flexibility of muscles and joints, faster and safer walking ability, less difficulty performing the tasks of daily living, and an overall higher quality of life.
Among the many exercise options is an agility program that incorporates the principles of tai chi, kayaking, boxing, lunges and Pilates. It was developed and proved safe and effective by Laurie A. King and Fay B. Horak at Oregon Health and Science University. The agility course includes navigating turns, doorways, hallways and small areas; tasks like walking with knees high and hands touching them; skipping; and shuffling from side to side.
In a report on their work in Physical Therapy, the journal of the American Physical Therapy Association, King and Horak explained that intense exercise can improve "plasticity" of the brain, protect against nervous system degeneration, and even reverse motor deficits.
Another program, called Rock Steady Boxing, was founded by Scott C. Newman, a former prosecutor in Marion County, Indiana, who developed Parkinson's at age 40. He reported significant improvements in his physical health, agility, daily functioning and quality of life shortly after he began high-energy workouts doing boxing moves a few years after his diagnosis.
While it is best to begin a challenging exercise program early in the disease, Moffat and Newman say it can help at any stage. Rock Steady Boxing has created training programs suited to fitness levels at all stages of Parkinson's.
Another personal experience, by a cross-country cyclist, resulted in a tandem cycling program for Parkinson's patients. In a 200-mile trip across Iowa in 2003, Jay Alberts, a biomedical engineer at the Cleveland Clinic, pedaled in the lead position with a woman who has Parkinson's. The pace he set forced her to pedal a third faster than she would have done on her own. The woman's tremors disappeared while she was pedaling with Alberts, and he later showed in a controlled study that the ability of forced pedaling to suppress Parkinson's symptoms can persist for weeks afterward.
The exercise program that has mainly helped Sills, called LSVT BIG, evolved from the Lee Silverman Voice Treatment program - LSVT LOUD - created to improve the speech of Parkinson's patients, who tend to talk more and more softly. Developed specifically to counter the unique movement impairments associated with Parkinson's, it trains patients to "make big strong movements, not little weak ones," Sills said, for example, taking big steps and swinging your arms widely when you walk. "This is the normal way to walk, but not when you have Parkinson's, but it no longer feels strange to me," she said.
Other programs tailored to benefit Parkinson's patients include ParkFit, which fosters a more active lifestyle; Dance for PD, which has classes in New York City and many other countries; and Microsoft Kinect Adventures, which uses Xbox games geared to different stages of the disease.
http://www.heraldtribune.com/news/20170131/brody-exercise-early-and-often-counters-parkinsons

Monday, January 30, 2017

Boxing class fights back against Parkinson's

January 30, 2017
BATON ROUGE, LA (WAFB) -



A group of Baton Rouge boxers is taking on a scary opponent – Parkinson’s disease.


Rock Steady Boxing is a nonprofit with affiliates around the country. The Baton Rouge class was the first in Louisiana, and the program has since popped up in New Orleans, Slidell and Ruston. Others are in the works in Hammond and Shreveport.

 “It's hand-eye coordination, agility, teaching them how to fall, how to get up and fall, because that's a big part of it. You lose your balance a lot (with Parkinson’s),” coach Melissa Cantrell explained.

“I started with a tremor in my right hand and tried to ignore it, but eventually I had to address it,” Rock Steady boxer Sally Palmer said. She’s been in the class since it launched in May 2016.

Palmer’s doctor told her that getting regular exercise is just as important as taking her daily medications. Studies have shown that rigorous, non-contact boxing can delay, reduce and even reverse the symptoms of Parkinson’s.

“To see people come in that really didn't think they could do something anymore, and to see them accomplish that, it's fantastic,” Palmer added.

The benefits are not just physical. The class doubles as a support group, helping fight the depression that often comes with the disease. It’s something Cantrell experienced personally with her parents, and it’s what motivated her to offer the class.

“You kind of start taking away everything that's important,” she explained. “My mom likes to bake, she's a cook. My dad's yard work. They're both retired, and so you see those little things that they can't do anymore.”

Rock Steady is about what they CAN do. Calisthenics are mixed in with the boxing for an hour of balanced exercise. Cantrell assesses each participant before they begin the class, and then reassesses each person every six months. A doctor’s approval is recommended but not required.

“We have early-onset from late 30s all the way up – there's a lady I think she's in Indiana, she's in her 90s, so there's no age limit on this,” Cantrell said. Anyone is welcome to come observe the class before signing up.

Rock Steady Boxing meets every Tuesday and Thursday from 11 a.m. – Noon at the Southside YMCA located at 8482 Perkins Rd. Call (225) 766-2991 for more information.

Palmer also leads a Parkinson's support group that meets at 1 p.m. on the third Thursday of each month. Meetings are at the Bluebonnet branch of the EBRP Library.
http://www.kplctv.com/story/34363734/boxing-class-fights-back-against-parkinsons

Nurse-led nursing home service for Parkinson’s disease in running for award

January 30, 2017    BY 

The finalists have been announced for the first ever awards scheme designed to showcase pioneering and outstanding services for patients with Parkinson’s disease.



A nurse-led nursing home service, a multidisciplinary unit and a quality improvement team are all in the running for an award from the network set up by charity Parkinson’s UK.
“I know these finalists represent the tip of a much larger iceberg of the quality care provided”
David Burn



The UK Parkinson’s Excellence Network is a collaboration between health and social care professionals, the charity and patients with the long-term neurological condition.
Launched in 2015, it encourages professionals to work together for change, build an expert workforce, influence services and strengthen the voice of people affected.
The new awards, which are the first of their kind, aim to recognise and celebrate outstanding services that make a difference to people in the UK affected by Parkinson’s disease.
Of more than 40 entries, seven finalists have been chosen to be recognised as part of the inaugural awards ceremony at the Positive Steps conference in Leicestershire on 3 March.
The finalists for the 2017 UK Parkinson’s Excellence Network Awards are:
  • Heart of England Foundation Trust Parkinson’s Quality Improvement Team
  • Cardiff and Vale University Health Board’s Parkinson’s Clinic
  • Parkinson’s Advanced Symptoms Unit (a collaboration between South Tees NHS Trust and Tees, Esk and Wear Mental Health Trust)
  • Neurology Parkinson’s Service at Plymouth Hospitals NHS Trust
  • Parkinson’s Nurse-led Nursing Home Clinic at Cardiff and Vale University Health Board
  • The Coventry and Warwickshire Regional Parkinson’s Service
  • Parkinson’s Service at Derby Teaching Hospitals NHS Foundation Trust
Professor David Burn, clinical director of the network, said: “We have been overwhelmed by the quality of entries for our first ever Excellence Network Awards.
“I know these finalists represent the tip of a much larger iceberg of the quality care provided,” he said. “I would like to congratulate every service that has reached this stage.
“It is a momentous achievement to be recognised as a finalist on a national level for sheer dedication and support for people with Parkinson’s. I look forward to celebrating all of these finalists at the awards ceremony in March,” he added.

https://www.nursingtimes.net/news/charities/nurse-led-parkinsons-service-in-running-for-award/7015228.article?blocktitle=Today

Sunday, January 29, 2017

Catherine inspired to take on charity challenge

January 29, 2017



AN ADRENALINE junkie has jumped from a plane to raise money for a charity close to her heart.
Catherine Holcombe from Shipston took part in a tandem skydive to raise money for Parkinson’s UK after her mother-in-law Jean died from the disease.
The 42-year-old told the Observer: “Jean was such an amazing lady – strong, independent, and was always doing good deeds for others.
“Suffering with Parkinson’s meant she lost a lot of her independence in later years and had to give up many of her hobbies and Shipston community activities, in which she was always so active.
“My skydive doesn’t seem much when I reflect on the good deeds Jean did for so many people but I wanted to do something to support this amazing charity and the many sufferers of this hideous disease. I also wanted to do something in her memory. A skydive is something I’ve always wanted to do but was simply never brave enough.”
And after being terrified to do the jump, Catherine has now fallen in love with the experience and cannot wait to go again.
From this jump she hopes to raise £1,000 for the charity, and is currently just £200 off her target.
Catherine said: “Parkinson’s UK is an amazing charity and I’m thrilled to bits to have been able to do something to help raise much needed funds.
“I’m still hoping to reach my target as that amount would fund a week long research project to help find a cure.”
Visit uk.virginmoneygiving.com/CatherineHolcombe to donate.

https://stratfordobserver.co.uk/news/catherine-inspired-to-take-on-charity-challenge/