Parkinson's disease sufferer rowing across Indian Ocean for groundbreaking study

By Laura Meachim     Posted July 06, 2018

Photo: The crew of four hope to beat the world record of 68 days to row from Geraldton to Mauritius. (Supplied: Peter Frankland)

Four men from the United Kingdom are hoping to break a world record while participating in groundbreaking Parkinson's disease research — by rowing non-stop for 1,900 hours across the Indian Ocean.

Photo: Robin Buttery faces his biggest challenge yet, overcoming the symptoms of his Parkinson's disease to row across the Indian Ocean.  (ABC Midwest and Wheatbelt: Laura Meachim)

It is a feat successfully completed by only half of those who have attempted it: rowing 5,700 kilometres from Western Australia to Mauritius in a 29-foot boat.

But the No Great Shakes crew are rowing for a different reason — they are taking part in a world-first study on how ongoing exercise can affect someone with Parkinson's Disease.

Robin Buttery was diagnosed with young onset Parkinson's disease just before his 44th birthday.

While his diagnosis was a challenge, he said rowing the Indian Ocean would be in a totally different league. 

"I want people to see how something like this affects somebody with Parkinson's disease so they should see the good, the bad and the ugly," he said.

"It is obviously putting myself on show a little bit, but I want them to see how it affects me compared to somebody who is able-bodied and fit."

Mr Buttery said he rowed occasionally in his youth, but the stretch across the Indian Ocean was expected to take more than 60 days to complete.

"Just under 48 hours is the longest I have been rowing on the sea as one stint," he said.

"So I am definitely the novice of the crew, some would say I am mad but I am definitely keen to push myself."

Photo: The No Great Shakes maiden voyage in Guernsey was its longest to date, the crew were at sea for 48 hours.  (Supplied: Peter Frankland)

A first for Parkinson's researchers

Researchers from Oxford Brooke University will monitor Mr Buttery and the crew's skipper Billy Taylor, who does not have Parkinson's as a control.

Photo: Skipper Billy Taylor said it felt good to know their journey could potentially help those with Parkinson's disease.  (ABC Midwest and Wheatbelt: Laura Meachim)

Senior clinical research fellow Johnny Collett said this was the first time this type of physical challenge had been researched for Parkinson's disease.

"We suspect that this is the first time researchers have come across anyone with Parkinson's wanting to row an ocean," Dr Collett said.

"It is a rather niche pastime.

"But anecdotally, people with Parkinson's who have done extensive amounts of exercise have reported it benefits their Parkinson's."

Researchers have spent the last year assessing Mr Buttery and Mr Taylor, who are both the same age.

They will collect information, using cameras fitted to the boat, while the crew are at sea.

Dr Collett said the research aimed to see whether repetitive exercise was beneficial to those with the disease.

"We will assess them again after the row to see how the exercise and repetitive action of rowing has effected their cardiovascular and metabolic systems," he said.

The results will be used in the university's ongoing research program into Parkinson's disease, with the hope of helping improve the lives of those living with the condition.

Photo: The four-man crew will call this 29-foot boat home for the next 60 days. (Supplied: James Plummley)

A personal challenge

Two other experienced crew members will join Mr Buttery and Mr Taylor on the journey — Barry Hayes and James Plummley, who in 2013 was part of a record-breaking team who were the fastest to row non-stop around the UK coastline.

Photo: Robin Buttery and Billy Taylor will be monitored across the voyage, to see how consistent exercise affects someone with Parkinson's disease. (ABC Midwest and Wheatbelt: Laura Meachim)

Mr Buttery said, despite having an experienced crew supporting him, he would likely find the journey difficult.

"Obviously, I am going to have struggles with tremor," he said.

"All extremes can bring on tremor — cold, physical exercise can bring on tremor, so that is definitely going to happen.

"Cramps are something I get and I know I will get those while rowing extensively."

The crew will row non-stop day and night on a two-hour-on, two-hour-off shift pattern with no support crew. 

Sleep deprivation and exhaustion are things that could affect the crew, but that is the least of their worries with extreme weather conditions, tanker vessels, whales and sharks likely to meet them along the way.

http://www.abc.net.au/news/2018-07-06/no-great-shakes-mission-to-row-the-indian-ocean-for-parkinsons/9932242

Rethinking neurodegenerative disease treatment: Target multiple pathological proteins, not just one

July 5, 2018  

Perelman School of Medicine at the University of Pennsylvania

Nearly all major neurodegenerative diseases—from Alzheimer's to Parkinson's—are defined and diagnosed by the presence of one of four proteins that have gone rogue: tau, amyloid-beta (Aβ), alpha-synuclein (α-syn), or TDP-43. As such, investigational drugs and studies aimed at preventing or slowing the disease often hone in on just one of these respective proteins. However, targeting multiple proteins—known as "proteinopathies"—at once may be the real key, according to a recent study published in Brain by Penn Medicine researchers.

These so-called "proteinopathies"—misfolded proteins that accumulate and destroy neurons—co-exist in varying degrees across all of the different neurodegenerative disorders and may instigate each other to drive disease severity in many aging patients. The prevalence of these co-pathologies suggests that each disease may ultimately require combination therapy targeting multiple disease proteins, and not just a single therapy, in patients with both early and later-stage disease.

"Historically, the focus of most clinical trials has been on targeting the primary pathological proteins of a given neurodegenerative disease such as deposits of tau and Aβ for Alzheimer's disease, but we see now that many of these disease-related aggregated proteins affect most older patients across a full spectrum of clinical and neuropathological presentations," said senior author John Q. Trojanowski, MD, Ph.D., a professor of Pathology and Laboratory Medicine and director of Penn's Institute on Aging. 

"This gives us additional leverage to find ways to detect patients' specific proteinopathies with increasingly sophisticated biomarker and imaging technologies. This will allow us, and other researchers, to better match participants with specific targeted therapies in clinical trials."

The study—which analyzed 766 autopsied brains at Penn's Center for Neurodegenerative Disease Research (CNDR)—revealed that patients with more severe forms of their diseases had more co-pathologies. Researchers also found that increased age and the presence of the APOE ε4 allele—a typical gene variant associated with an increased risk for late-onset Alzheimer's disease—are risk factors for co-pathologies.

The researchers studied patients with the following diseases: Alzheimer's disease, Pick's disease, corticobasal degeneration (CBD), progressive supranuclear palsy, multiple system atrophy, Parkinson's disease with and without dementia, dementia with Lewy bodies, as well as frontotemporal lobar degeneration with TDP-43, amyotrophic lateral sclerosis, and primary age-related tauopathy (PART).

While co-pathologies have been observed in Alzheimer's and Lewy body disease, tau, Aβ, α-syn, and TDP-43 co-pathologies are rarely reported in the other neurodegenerative diseases.

The CNDR researchers found that co-pathologies were common but varied among the disease groups, ranging from 27 to 81 percent of patients having co-pathologies. For example, 52 percent of patients with CBD, in which tau as the primary protein, had multiple other neurodegenerative disease protein deposits present.

Tau was nearly universal, with 92 to 100 percent of all patients having at least one form. Aβ was next, with 20 to 57 percent of patients having at least one type of protein deposit, while α-syn pathology, typically seen in Parkinson's disease, was less common, with 4 to 16 percent. TDP-43 deposits, which are characteristic pathological signatures of frontotemporal lobar degeneration and amyotrophic lateral sclerosis, were the rarest, with 0 to 16 percent of patients having these deposits.

In several neurodegenerative diseases, co-pathologies increased more considerably. For example, in patients with Alzheimer's disease (tau and Aβ deposits are the primary signatures), α-syn pathology—similar to that of a Lewy body—increased by up to 55 percent and TDP-43 by up to 40 percent.

The findings not only show a high prevalence of co-pathologies, but also suggest a patient's primary pathological protein may influence co-pathology prevalence and severity, as shown in patients with Alzheimer's and Lewy body disease patients.

The presence of multiple co-pathologies increased from 9 percent to 25 percent between intermediate Alzheimer's and higher-level Alzheimer's patients, and from 0 percent to 21 percent between brainstem- or amygdala-only Lewy body disease and the more aggressive neocortical Lewy body disease.

These findings support the "proteopathic seeding" hypothesis that has been previously established in model systems of neurodegenerative diseases. Misfolded proteins may directly "cross-seed" other normal, vulnerable proteins to accumulate and clump via a cell-to-cell transfer of toxic proteins.

"Our study is an important first step in understanding the extent to which co-pathologies present in and impact all neurodegenerative diseases," said co-author Virginia M.-Y. Lee, Ph.D., the CNDR director and a professor of Pathology and Laboratory Medicine. "Now we need to probe these protein-to-protein interactions more closely to better understand how they progress in patients' brains, with an eye toward clinical studies that combine targeted therapies to halt or slow accumulation of these disease proteins."

Journal reference: Brain 

Provided by: Perelman School of Medicine at the University of Pennsylvania 

https://medicalxpress.com/news/2018-07-rethinking-neurodegenerative-disease-treatment-multiple.html

Brain Cell That Improves Learning Detected

July 5, 2018
Source: Uppsala University.

A new study reveals OLM cell activity can affect memory encoding. The findings enhance understanding of how a single component in memory circuits can affect memory formation.

The same research group had previously discovered ‘gatekeeper cells’ or, in technical parlance, OLM (Oriens-lacunosum moleculare) cells. These are located in the hippocampus, the brain area known to be active in forming new memories. NeuroscienceNews.com image is in the public domain.

The workings of memory and learning have yet to be clarified, especially at the neural circuitry level. But researchers at Uppsala University have now, jointly with Brazilian collaborators, discovered a specific brain neuron with a central role in learning. This study, published in Neuron, may have a bearing on the potential for counteracting memory loss in Alzheimer’s disease.

When a person with dementia forgets having just eaten dinner, it is due to hippocampus damage. In contrast, the same person can describe in vivid detail a fishing trip to Norway 40 years ago. Both cases entail the use of episodic memory, the brain’s storage of events in which we have been personally involved. Dementia diseases impair the ability to form new memories, especially of events since the onset of the disease.

Researchers at Uppsala University have now, jointly with Brazilian colleagues, found certain neurons in the brain that play a crucial part in learning. The same research group had previously discovered ‘gatekeeper cells’ or, in technical parlance, OLM (Oriens-lacunosum moleculare) cells. These are located in the hippocampus, the brain area known to be active in forming new memories. The new findings from Klas Kullander’s research group show that OLM cells’ activity affects the encoding of memories in the brain.

When the OLM cells were overactivated in experiments on laboratory mice, the mice’s memory and learning functions deteriorated. When these cells were inactivated instead, the function of new memory formation improved. This research has enhanced understanding of how a single component in the memory circuits can affect memory formation.

“We had expected to be able to impair learning, since it seemed likely that the effect of our experiment at the cellular level would disturb the normal function of the nervous system. However, we were surprised to find that learning and memory also could be improved,” says Klas Kullander.

It also offers hope of being able to counteract the loss of memory formation in Alzheimer’s disease and dementia. The first symptoms of Alzheimer’s, the most common and familiar dementia disease, are associated with poor memory. Short-term memory is particularly impaired. For those who suffer from dementia symptoms, losing memory functions is a major everyday problem. Unfortunately, there are no curative treatments or medicines that can stop dementia diseases from developing.

“The next step is therefore to investigate this more closely, in further experiments on animal subjects comparable to humans. We need more knowledge before experiments can be done to stimulate the OLM cell artificially in humans,” Kullander says.

About this neuroscience research article

Klas Kullander, Professor at the Department of Neuroscience, researches neuronal circuitries and their functions. His international research group studies neuronal circuitries that are important for learning, memory, motor skills and cognition. The studies are conducted using methods in genetics, molecular biology and electrophysiology.

Funding: This study was supported by Swedish Research Council, Swedish Brain Foundation, Bissen Brainwalk Foundation.

Source: Klas Kullander – Uppsala University

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is in the public domain.

Original Research: The study will appear in Neuron.

https://neurosciencenews.com/learning-neurons-9516/

“Skinny Fat” in Older Adults May Predict Alzheimer’s Risk

July 5, 2018
Source: Florida Atlantic University.

Researchers say the combination of low muscle mass and strength in the context of high fat mass, could be a predictor of cognitive function in older adults. Sarcopenic obesity could be used to predict risk factors for developing dementia, the study reports.

James E. Galvin, M.D., M.P.H., tests a patient’s muscle strength in FAU’s Comprehensive Center for Brain Health. NeuroscienceNews.com image is credited to Florida Atlantic University.

A new study has found that “skinny fat” – the combination of low muscle mass and strength in the context of high fat mass – may be an important predictor of cognitive performance in older adults. While sarcopenia, the loss of muscle tissue that is part of the natural aging process, as well as obesity both negatively impact overall health and cognitive function, their coexistence poses an even higher threat, surpassing their individual effects.

The study, published in the journal Clinical Interventions in Aging, was led by researchers at Florida Atlantic University’s Comprehensive Center for Brain Health in the Charles E. Schmidt College of Medicine.

Using data from a series of community-based aging and memory studies of 353 participants, the researchers assessed the relationship of sarcopenic obesity or skinny fat with performance on various cognition tests. The average age of the participants was 69. Data included a clinic visit, valid cognitive testing such as the Montreal Cognitive Assessment and animal naming; functional testing such as grip strength and chair stands; and body composition (muscle mass, body mass index, percent of body fat) measurements.

Results from the study show that sarcopenic obesity or “skinny fat” was associated with the lowest performance on global cognition, followed by sarcopenia alone and then obesity alone. Obesity and sarcopenia were associated with lower executive function such as working memory, mental flexibility, self-control and orientation when assessed independently and even more so when they occurred together.

Using a cross-sectional design, the researchers found consistent evidence to link sarcopenic obesity to poor global cognitive performance in the study subjects. This effect is best captured by its sarcopenic component with obesity likely having an additive effect. This effect extends to specific cognitive skills, in particular executive function.

“Sarcopenia has been linked to global cognitive impairment and dysfunction in specific cognitive skills including memory, speed, and executive functions,” said senior author James E. Galvin, M.D., M.P.H., one of the most prominent neuroscientists in the country, associate dean for clinical research and a professor of integrated medical science in FAU’s Schmidt College of Medicine, and a professor in FAU’s Christine E. Lynn College of Nursing. “Understanding the mechanisms through which this syndrome may affect cognition is important as it may inform efforts to prevent cognitive decline in later life by targeting at-risk groups with an imbalance between lean and fat mass. They may benefit from programs addressing loss of cognitive function by maintaining and improving strength and preventing obesity.”

Obesity may contribute to the risk of impaired executive function through vascular, behavioral, metabolic, and inflammatory mechanisms or can result from reduced impulse control, self-monitoring, and goal-directed behavior in individuals with impaired executive function with a negative effect on the ability to maintain energy balance. The exact mechanisms linking obesity to cognitive dysfunction are yet to be determined, although several pathways including sedentary behavior, inflammation, and vascular damage have been proposed. Sarcopenia, in turn, has been linked to impairments in abilities that relate to conflict resolution and selective attention. Executive function is reduced in obese older adults, and improvement in muscular function has been linked to enhancement of executive function in senior adults.

Galvin and his study collaborators, Magdalena I. Tolea, Ph.D., a research assistant professor of integrated medical science, and Stephanie Chrisphonte, M.D., a research assistant professor of integrated medical science, both in FAU’s Schmidt College of Medicine, caution that changes in body composition including a shift toward higher fat mass and decreased lean muscle mass represent a significant public health concern among older adults as they may lead to various negative health outcomes including cardiovascular and neurodegenerative diseases.

“Sarcopenia either alone or in the presence of obesity, can be used in clinical practice to estimate potential risk of cognitive impairment,” said Tolea. “Testing grip strength by dynamometry can be easily administered within the time constraints of a clinic visit, and body mass index is usually collected as part of annual wellness visits.”

About this neuroscience research article

Funding: This study was supported by grants from the National Institute on Aging of the National Institutes of Health (R01 AG040211 and P30 AG008051), the Morris and Alma Schapiro Fund and the New York State Department of Health.

Source: Gisele Galoustian – Florida Atlantic University

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is credited to Florida Atlantic University.

Original Research: The study will appear in Clinical Interventions in Aging.

https://neurosciencenews.com/skinny-fat-dementia-9515/

Resources for Veterans

Veterans and Parkinson’s disease

Veterans may be at an increased risk of Parkinson’s disease (PD) because of their service. Evidence suggests that one cause of Parkinson’s disease may be exposure to pesticides or herbicides. During the Vietnam War, many veterans were exposed to Agent Orange, a mix of herbicides that was used by the US military to defoliate trees and remove concealment for the enemy. There are other causes of Parkinson’s disease as well, and most people who develop Parkinson’s disease were never exposed to high levels of pesticides or herbicides.

Education and Clinical Centers

The Department of Veterans’ Affairs (VA) established six Parkinson’s Disease Research, Education, and Clinical Centers or “PADRECCs”. Each PADRECC delivers state-of-the-art clinical care, conducts innovative research, and offers outreach and educational programs to all veterans currently enrolled in the VA Healthcare System. Eligible veterans include those who have been diagnosed with Parkinson’s disease and those who have just started to notice PD-like symptoms.

PADRECCs also treat veterans diagnosed with other movement disorders, like essential tremor. PADRECCs are located in Houston, TX; Los Angeles, CA; Portland, OR; Seattle, WA; Philadelphia, PA; Richmond, VA; and San Francisco, CA.

For veterans who cannot travel to a PADRECC, the VA more than 51 Consortium Centers—VA clinics that offer specialized Parkinson’s disease and movement-disorder specialty care. These Centers are staffed by movement disorder specialists or clinicians with vast experience and interest in the field of movement disorders. These VA Consortium Centers work collaboratively with the six PADRECCs to ensure the highest level of care for all veterans.

To Download: please go to :

https://d2icp22po6iej.cloudfront.net/wp-content/uploads/pdf_publications/Helping-Those-Who-Serve-Parkinsons-Disease-Information-For-_Tg.pdf

For more information, call the PADRECC/Consortium Hotline at 800-949-1001, x5769 or visit their website www.parkinsons.va.gov

The Department of Veterans’ Affairs (VA) established six Parkinson’s Disease Research, Education, and Clinical Centers or “PADRECCs”. Each PADRECC delivers state-of-the-art clinical care, conducts innovative research, and offers outreach and educational programs to all veterans currently enrolled in the VA Healthcare System. Eligible veterans include those who have been diagnosed with Parkinson’s disease and those who have just started to notice PD-like symptoms.

PADRECCs also treat veterans diagnosed with other movement disorders, like essential tremor. PADRECCs are located in Houston, TX; Los Angeles, CA; Portland, OR; Seattle, WA; Philadelphia, PA; Richmond, VA; and San Francisco, CA.

For veterans who cannot travel to a PADRECC, the VA more than 51 Consortium Centers—VA clinics that offer specialized Parkinson’s disease and movement-disorder specialty care. These Centers are staffed by movement disorder specialists or clinicians with vast experience and interest in the field of movement disorders. These VA Consortium Centers work collaboratively with the six PADRECCs to ensure the highest level of care for all veterans.

Agent Orange

Veterans exposed to Agent Orange during military service may be eligible for a free Agent Orange Health Registry Exam. Registry health examination, healthcare benefits, and disability compensation. Vietnam veterans with Parkinson’s disease or other diseases possibly associated with Agent Orange may claim benefits without having to prove that their conditions are due to Agent Orange exposure.

For more information please visit:

U.S. Department of Veteran’s Affairs, Agent Orange Exposure

Or, call 800-749-8387, x3. Ask about registry health examination, health care benefits, and disability compensation.

Information and services can change. Please check the Veteran’s Administration website for the most accurate and up-to-date information.

https://www.apdaparkinson.org/resources-support/national-veteran-resources/

As Science Catches Up with Decades of Anecdotal Evidence that Dance...

By Byron Wood   July 4, 2018

It's one thing to read an article in a medical journal about how dancing can assuage the symptoms of Parkinson's disease. But Susan Saenger, a dance and movement therapist with the American Dance Festival's Parkinson's Movement Initiative, was watching it happen right in front of her.

She and occupational therapist Lindsay Voorhees were teaching their Dance for Parkinson's class at Broad Street Studios, using the soundtrack from The Music Man. At the end of the session, one student found she couldn't leave. She was "frozen," a Parkinson's condition in which the person's feet feel glued to the ground.

"Well, march out," Saenger said, and started singing "76 Trombones." The student immediately walked out of the room. The instructor's unconventional request lifted an everyday movement out of the woman's subcortex, where habitual gestures like walking are stored, and into the problem-solving cortex, a part of the brain unaffected by Parkinson's.

"Anything that demands a new physical response is an answer to the problem," says Voorhees. "We ask, 'Can you get from here to that counter to take your pills if you think of it as a dance?' And people have said yes." Voorhees hastens to add that it doesn't work all the time, and that dancing doesn't represent a cure for the world's second-most common neurological disease, which affects some six million people, most over age sixty.

But dance "is one of the most immediate things that we know can really help people in their lives," Saenger says. "We already know a lot about what can enhance quality of life, and finding movement you love and engage in consistently—we know that works."

Science has been catching up with the anecdotal evidence suggesting that dance can not only make people with Parkinson's feel better but also reduce the severity of their symptoms. Over the last decade, dozens of peer-reviewed articles have found that dancing can improve the motor and cognitive functions, mental symptoms, and quality of life among people with Parkinson's.

In 2001, the Brooklyn Parkinson's Group proposed a dance class for its patients to the Mark Morris Dance Group, already one of the top modern dance companies at the time. As the classes' popularity spread—and research began confirming its medical effects—the company's Dance for Parkinson's program spread to two hundred and fifty communities in twenty-four countries.

Duke student Alana Jackson founded NC Dance for Parkinson's during her senior year in 2013, and recruited Voorhess and Sanger over the following years, first as volunteers, then as teachers. Last year, ADF began coordinating that effort with those of Poe Wellness Solutions into a cohesive program of weekly free classes at the festival's Broad Street Studios. A grant from the Parkinson's Foundation, with funds from its annual Moving Day North Carolina walkathon in Raleigh, made the series possible, including Saenger and Voorhees's dance classes, Pilates for Parkinson's, and workshops and outreach classes in Tai Chi and physical and music therapy.

According to Julia Pleasants, ADF's community engagement manager, the initiative reached more than one hundred and thirty people in its first year, which concluded in late June with a workshop in Argentine tango led by local dancer and Culture Mill codirector Murielle Elizéon, who is also the only local choreographer on ADF's mainstage season (see sidebar). The festival has applied for funds to continue the program after its summer hiatus.

Saenger, Voorhees, and Pilates instructor Meg Poe resist labeling their classes as therapy.

"People with Parkinson's are always going to therapy," Saenger says. "Their lives are filled with doctors' appointments. They don't want another therapy. They want to feel like they're just living their lives."

That makes the ADF classes "the anti-therapy," a room where people can leave Parkinson's—and their usual roles as patients and caregivers—at the door. Voorhees says the teachers attempt to "create a space where there is freedom from the limitations that Parkinson's can impose on the mind and body." That space also has to suspend the judgments found in ordinary exercise classes.

"It takes the stress of, 'Am I doing it right?' away and allows all of us to be in our own bodies however we can," Saenger says. "In this class, there is no Parkinson's, and no observers. There are only dancers." She pauses for a moment, grins, and adds, "There are no mistakes. There are only solos."

How rare is such an environment for people with Parkinson's? A student in Poe's Pilates class told her, "This is the first time I felt I belonged somewhere in six months." Paula Easton, a neighborhood coordinator with Fearrington Cares, says the ADF classes have been "the beginning of a turnaround for me. When I left that first class, I called a friend and said, 'This is the most wonderful thing I could have found.'"

Easton believes the classes have helped her keep her Parkinson's at bay. "My muscle movement is better, my control of movement is better, my stiffness and muscle weakness are improving, and it helps with my body awareness. I just feel more in control of my movement and everything I do."

https://www.indyweek.com/indyweek/as-science-catches-up-with-decades-of-anecdotal-evidence-that-dance-helps-people-with-parkinsons-disease-local-efforts-converge-at-adf/Content?oid=15663295

Toward a better understanding of Parkinson's disease

July 4, 2018

Immunohistochemistry for alpha-synuclein showing positive staining (brown) of an intraneural Lewy-body in the Substantia nigra in Parkinson's disease. Credit: Wikipedia

A new study, published today in Nature Structural and Molecular Biology, moves researchers closer to understanding one of the crucial proteins involved in Parkinson's disease.

Parkinson's disease is the second most common neurodegenerative disease and commonly affects patients over 60 years of age. It is caused by the degeneration of neurons that are located in the mid-brain and are involved in the dopamine system. One of the causes of the disease is the failure to clear away the damaged mitochondria within these neurons. Mitochondria are the powerhouse of the cells, creating energy for the cell. 

Mutations in a protein, parkin, are responsible for a genetic form of the disease. Now, by using powerful beams of x-rays, a McGill-based research team, led by Kalle Gehring, has been able to visualize the steps of activation of this crucial protein. With funding from the Michael J Fox Foundation and the Canadian Institutes of Health Research, the team is learning how parkin is regulated within cells. This research offers hope for using parkin as a target for therapeutic agents to slow or prevent the progression of Parkinson's disease.

More information: Véronique Sauvé et al. Mechanism of parkin activation by phosphorylation, Nature Structural & Molecular Biology (2018). DOI: 10.1038/s41594-018-0088-

Journal reference: Nature Structural & Molecular Biology 

 Nature Structural and Molecular Biology

Provided by: McGill University 

https://medicalxpress.com/news/2018-07-parkinson-disease.html

How to Deal with the 3 Common Causes of Leg pain in PD? By " Dr. De Leon"

By " Dr. De Leon"  by defeatparkinsons    July 2, 2018

Image/artwork by Ros Webb

One of the biggest complaints I hear from people in PD support groups is a continuous relentless severe leg pain. Prior to a decade ago, I as all my fellow movement disorder specialist would have not thought leg pain to be a direct precursor of PD or an initial non-motor symptom. My grandmother often complained of pain and deep aches in her calves and in her legs which started before her tremors and shuffling were noticeable. But, I was unaware of the connection at the time and erroneously assumed her pain was neuropathic in nature due to her diabetes but was always somewhat surprised that she continue to complain of this pain on and off throughout her illness despite neuropathic medication. With hind sight what she was experiencing was central pain of PD. I too had severe pain first in one leg then the other which would come on suddenly without warning stopping me in my tracks throughout the day. I was constantly asking my husband to massage my legs just as my grandmother had asked of us time and time again.

So why do we have leg pain in PD and what can we do to relieve the discomfort? 

First, some believe that lower limb pain is a specific non-motor phenotype variant of central pain in Parkinson’s disease. I, too, believe this; more importantly it can be one of the very first signs of PD as it was for me. This pain is usually bilateral.

Second, leg pain can also occur secondary to dystonia as an initial symptom or as a consequence of long term levodopa use (most common). When related to levodopa it usually occurs as a wearing off but can also occur at peak dose. In most cases this leg pain is unilateral and has direct correlation to medication intake. When is due to dystonia pain is more common in early morning. This type of leg pain is usually accompanied by toes curling and foot abnormally posturing.

Third, musculoskeletal pain due to rigidity, abnormal posturing and lack of mobility affects legs commonly causing pain in the legs, however this pain is usually more pronounced on the more affected side. 

TREATMENTS:

Treatments therefore depend on properly identifying the source of pain.

• If bilateral always assume it is central pain- pain due to PD and treat accordingly. As I mentioned many times before, Azilect works great for this type of pain.

• Massage therapy works for all types of leg pain-my favorite.

• If having pain due to dystonia first find out if occurring at end of dose or at peak dose so medications can be adjusted. If medication adjustment don’t work consider DBS. Pain due to dystonia also responds well to Botox injections, centrally acting muscle relaxants alone or in combination with other treatment modalities. Physical therapy (PT) can go a long way to alleviating pain of this type.

• To avoid and alleviate pain caused by stiff muscles the best treatment is activity in the form of stretching exercises- any number of activities will do such as tai-chi, yoga.

• Lastly, don’t forget to stay well hydrated.

After traveling from coast to coast last few weeks, I too have experienced once again severe leg pain, something I have not had in a year at least. So, now that I am back home I can get a nice massage (thanks to friend’s thoughtfulness), rest, put my legs up, restart my exercise routine and increase my hydration.

Happy Fourth of July everyone!!!

P.s thank you for nominating me for Best in show Blog #WEGOHEALTHAWARDS – it is a true honor to represent the Pd community. if interested you can check out my profile there and vote for me or nominate someone else. Thank you for opportunity of letting me serve you and represent you.

parkinsonsdiva – WEGO Health Awards Nominee.html

@copyright 2018all rights reserved by Maria De Leon

https://defeatparkinsons.com/2018/07/02/how-to-deal-with-the-3-common-causes-of-leg-pain-in-pd-by-dr-de-leon/comment-page-1/#comment-7521