It’s Important to Avoid Dehydration with Parkinson’s


The other day I did something stupid. Really stupid. 

I love to putter in my garden on beautiful days. Only on this beautiful day, I crossed the line. My puttering turned into work, and before long, I was sweating bullets — shotgun-sized bullets on a 98-degree day.

Yet, I kept going. 

I kept going because I didn’t have the good sense to step back, sit down, take a rest in the shade, and get a drink. Like the Energizer Bunny, I just kept going and going and going. If my neighbor hadn’t come outside and reprimanded me (in a kind and concerned way), I’m honestly not sure what would have happened. I noticed while talking to her that I was stumbling around, slurring my words pretty badly, and sweating cats and dogs.

I promised her I would go inside and get some water and cool down. And I did. But I had pushed the boundaries a bit too far. 

During my last visit to the neurologist, my Medtronic rep for deep brain stimulation was talking to me, coincidentally, about how important it is to stay hydrated with a disease like Parkinson’s. He said the body is made up of approximately 60 percent water, and the brain 75 percent. For the brain to be healthy, it needs water. Lots and lots of water.

That day in my garden, I was starving my brain of what keeps it running at peak performance: water.

Water is important for all body functions.

The health advocates at That Sugar Movement note that, “Water is required by every cell in the body and important for all body functions. It helps transport oxygen and nutrients critical to the brain for optimal function, whilst providing cushioning and lubrication to the brain tissue. … So, staying hydrated is one critical factor for supporting the brain.”

Dehydration also can make you tired, mess with your cognitive abilities, lower your blood pressure, and force the brain to work even harder than a hydrated brain to do the exact same thing.

It took me over two days to bounce back from that episode, and it scared me enough to hopefully never repeat it again. With Parkinson’s disease, we’re dealing with major brain issues already. Adding self-inflicted dehydration to the mix is just plain stupid.

Take it from me. Learn from my mistake and go have a nice cold glass of water.


Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

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Senior Helpers Sending 6 Rock Steady Boxing Coaches from North Carolina to Group’s Conference

Rock Steady Boxing conference

Aware that non-contact boxing routines can improve the lives of Parkinson’s patients, Senior Helpers is sending six Rock Steady Boxing (RSB) coaches to the organization’s national conference.

Senior Helpers, a leading nationwide provider of at-home care, will sponsor the Wilmington, North Carolina, coaches in attending the second annual Rock Steady Boxing Coaches Conference to be held Sept. 4–6 in Phoenix.

At the conference, Rock Steady-certified coaches from around the world will learn the latest in techniques and practices. The non-profit Rock Steady Boxing uses a non-contact boxing-based fitness curriculum to help slow Parkinson’s progression and enable patients to better manage disease symptoms.

“As a care-based company, we understand firsthand how important it is to stay current with the skills and techniques that help our clients,” Mari Baxter, senior vice president of operations for Senior Helpers, said a press release.

“Rock Steady Boxing has been one of our most valued partners the past several years and the organization’s commitment to helping improve the lives of Parkinson’s patients is an exemplary example of humanitarianism,” Baxter added. “It’s our honor to help these coaches advance their skillsets and enhance their instruction.”

In general, research shows that exercise helps Parkinson’s patients maintain the abilities needed for a degree of independence in everyday life. In particular, exercises that stress gross motor movement, core strength, balance, and rhythm can positively affect patients’ range of motion, gait, posture, and flexibility.

The Senior Helpers-sponsored coaches are Mike Wilson, co-founder of Rock Steady Boxing of Wilmington and a former Jiu-Jitsu instructor; martial artist Val Wilson, who co-founded Rock Steady Boxing of Wilmington; Christy Gillenwater, a fitness studio owner who is certified as both a personal trainer and medical fitness specialist; multi-sport athlete Ryan Gillespie, a health and wellness veteran; Sheryl Johnson, a former police officer who was diagnosed with Parkinson’s in 2013; and Jim Cosper, a U.S. Navy veteran and Parkinson’s patient.

“Parkinson’s disease hits close to home for so many people, myself included,” Baxter said. “My husband Bill was recently diagnosed with Parkinson’s disease and has found Rock Steady to be an immense help in his overall wellbeing and day-to-day health. He was so resistant after his diagnosis, but now he’s their biggest convert.”

Founded in 2006 as the nation’s first boxing program of its kind, RSB is specifically designed to help patients at all stages of Parkinson’s. Visit this site to find a local class.

With more than 300 franchised businesses, Senior Helpers was founded in 2001 to help senior citizens with age-related illnesses and mobility challenges remain in their home.

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With BlueRock Acquisition, Bayer Plans to Open Trial of Cell Therapy for Parkinson’s

Bayer, BlueRock Therapeutics

Bayer has announced an agreement to acquire the cell therapy company BlueRock Therapeutics, and plans to open a clinical trial of a potential Parkinson’s stem cell-based treatment this year.

BlueRock, which will remain an independent entity under the plan, has a portfolio that focuses on engineered stem cell therapies to treat illnesses in the fields of neurology, cardiology and immunology.

Its lead program is in Parkinson’s, where preclinical work using BlueRock’s induced pluripotent stem cell (iPSC) technology has shown motor function improvement and higher dopamine production by stem cell-derived dopamine-producing neurons — those that are typically lost in distinct brain regions of Parkinson’s patients.

iPSC are derived from either skin or blood cells that have been reprogrammed back into a stem cell-like state, allowing for the development of a ready source of any type of human cell needed for therapeutic purposes.

According to Bayer, stem cell therapy could help reverse nerve cell degeneration by re-innervating the human brain and restoring motor function to people with Parkinson’s. Patients with multiple sclerosis, Alzheimer’s, Duchenne muscular dystrophy, congestive heart failure, and systemic lupus erythematosus may also benefit from BlueRock’s CELL+GENE platform, as the technology is called. It is designed to develop, manufacture, and deliver cell therapies with high purity, potency, and specificity.

Once the agreement in finalized, Bayer will own full rights to the iPSC technology, gene engineering, and cell differentiation capabilities of CELL+GENE.

“This acquisition marks a major milestone on our path towards a leading position in cell therapy,” Stefan Oelrich, a member of Bayer’s board of management and president of its Pharmaceuticals Division, said in a press release. “In line with our strategy to ramp up our investments in technologies with breakthrough innovation potential, we have decided to build our cell therapy pipeline based on BlueRock Therapeutics’ industry-leading iPSC platform.”

The agreement stems from a joint venture the Leaps by Bayer unit formed with Versant Ventures, setting up BlueRock in 2016. Leaps helps companies to become established and invests in early stage technologies with a potential to better treat, prevent, or cure major health concerns.

Bayer will acquire the remaining stake in the U.S.-based company for about $240 million in the coming months, with an additional $360 million to be given upon achievement of development milestones. The investment corresponds to a total BlueRock value of nearly $1 billion, according to the release.

Bayer’s support, said Emile Nuwaysir, PhD, BlueRock’s CEO, will aid its efforts to “pursue the discovery, development and commercialization of revolutionary new cell therapies” for patients with diseases “previously thought of as intractable.”

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With Parkinson’s, a Suntan Just Isn’t Worth It

heat intolerance

Betty slapped George hard. There was no response, so she dialed 911.

Parkinson’s disease (PD) had forced George into early retirement. He loved basking in the sun, diving into a good book, and working on his tan on their deck. Betty was in the kitchen when she saw him slumped over in the chair.

This wasn’t the first time George had responded so severely to the summer heat. He had reacted similarly to the heat two other times. His heart rate was slow, almost imperceptible. His face was ashen. Betty cradled George’s face in her hands as she waited for the ambulance, and with tears streaming down her face, commanded, “Don’t you die on me.” To herself, she said, “The suntan isn’t worth it.”

Similar stories are reported by many PD patients and their families.

Like George, the heat hits me hard. A small increase in air temperature above 75 degrees can leave me prone for hours, if not the entire day. Relief isn’t found by staying still or avoiding activities. I can have a difficult time in the shade or even in the house if the temperature rises.

I follow the recommendations to avoid heatstroke: I hydrate with water; complete any outside activities in the earlier, cooler parts of the day; and wear light, loose clothing. Our house is cooled by central air.

Despite all of these precautions, I can sense the losing battle with the heat as it rises. A comfortable summer day for others becomes a debilitating challenge for me due to heat attacks. This reaction to heat is an attack on my ability to function, a magnified response, such as my descriptions of fatigue and pain.

Researchers claim that heat intolerance is different than heat illnesses like heatstroke. Heat intolerance is usually a side effect of medications or a symptom of endocrine disorders or other medical conditions, rather than the result of too much exercise or hot, humid weather.

Up to 64 percent of PD patients report thermodysregulation, which includes symptoms of heat and cold intolerance as well as excessive sweating. PD patients have problems with their autonomic nervous system, which controls sweating. While perspiration helps regulate the body’s temperature, too much or too little perspiration can result in overheating.

Last month was the warmest July ever. It also included the worst bout of heat attacks ever recorded. It’s time for a tweak in the wellness map.

I’m trying to shift from thinking that I can work in some heat to understanding that it’s not worth the suntan. It’s not something to ignore or push through, distracting the mind from the physical issues, like hiding one’s head in the sand. It must be met straight on with reason and sensible action. Most of us are not yogi masters who can change body temperatures at will. We must use what we know and take steps to prevent serious harm from happening.

This is me telling myself not to take this risk lightly. I tend to push myself too hard.

The symptoms of heat intolerance can vary from person to person, but may include:

  • feeling very hot in moderately warm temperatures
  • excessive sweating
  • not sweating enough in the heat
  • exhaustion and fatigue during warm weather
  • nausea, vomiting, or dizziness in response to heat
  • changes in mood when too hot

If you experience any of these symptoms, time to get out of the heat! It’s just not worth the suntan.


Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

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Scientists Develop Simple, Affordable Way to Measure Tremors in Mice Using Smartphones

tremors, smartphone

Neuroscientists have developed a simple and inexpensive way to measure tremors, one of the main symptoms of Parkinson’s disease, in lab mice using a smartphone.

The new test showed comparable results to those generated with the expensive lab equipment currently used — opening a faster and more affordable way to test potential approved and investigational medicines, the scientists said.

“I thought it would be a pity if expensive equipment kept us from continuing our research to find treatments for tremor,” Eva Maria Meier Carlsen, the neuroscientist at the University of Copenhagen behind the new device, said in a press release. “That’s why I set out to find an affordable and valid way to measure it, and I came up with the idea of using a smartphone as a measuring device.”

Tremor is a common symptom of many neurological disorders, such as Parkinson’s disease, multiple sclerosis, and spinal cord injury. Although it greatly affects the quality of life of many patients, available treatments are few and non-specific. Tremor also is rarely measured in experimental mice because the required lab equipment is expensive, costing anywhere between $15,000 and $19,500.

Carlsen, a postdoctoral fellow at the university, came up with a simple solution: a smartphone. The method takes advantage of the accelerometer inside the phone — a device which detects tilt, motion, and acceleration, allowing the smartphone to tell up from down. The accelerometer is used in a phone’s compass function.

By fixing the smartphone to a cage suspended by rubber bands, Meier Carlsen and colleagues were able to measure the faint vibrations of the cage as the mouse trembled. In collaboration with Saniona, a company developing medications for the central nervous system, they determined that the accuracy of the new method was comparable with that of expensive commercially available equipment.

“It is a really good idea that Eva got, and our new study emphasizes its validity,” said Jean-François Perrier, associate professor at the Department of Neuroscience and head of the research project. “It is a good example of how we researchers sometimes have to challenge the conventions and invent new methods that are more accessible and can be used by more people.”

Meier Carlsen pointed out that the new method could be made even more affordable by omitting the smartphone entirely, and instead using a single-board computer — a small computing device fitted with an accelerometer.

The neuroscientists already are using this new method to test experimental medications for tremor in mice. They also plan to use it to test already approved therapies. If any of these proved effective, they could reach patients much sooner, the scientists said.

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Parkinson’s UK Awards Scientist £100,000 to ID Ways of Protecting Dopamine-producing Neurons

Parkinson's UK grant

A scientist at the University of Sheffield in England has been awarded a £100,000 grant by Parkinson’s UK to develop a treatment that might slow or stop the progression of Parkinson’s disease and protect brain cells.

The one-year grant, worth about $120,000, was given to Heather Mortiboys, a senior research fellow at the university’s Institute for Translational Neuroscience (SITraN), by Parkinson’s Virtual Biotech Programme, the British charity’s therapeutic development arm.

“All the clinical treatments for people living with Parkinson’s at the moment are based on easing these sometimes devastating symptoms,” Mortiboys said in a press release. “With this new funding award … we have the potential to go on to develop a drug treatment which will actively address the root cause of these symptoms to slow, or halt the progression of Parkinson’s for the first time.”

Mitochondria, power factories for cells that include dopamine-producing brain cells, don’t work as they should in people with Parkinson’s disease.  Resulting shortages in cellular energy cause neurons to fail and ultimately die, particularly dopamine neurons. Those nerve cells are responsible for movement and coordination, and rely on mitochondria to function.

In her previous work, Mortiboys developed a model of dopamine brain cells — using skin cells from patients — that allows researchers to test potential therapies. Her research team was able to grow high numbers of brain cells derived from these skin cells. They used them to identify compounds that support dopamine neurons and their mitochondrial function, and potentially lessen cell death.

With this award, Mortiboys and her team will try to pinpoint the molecules in these compounds that are of greatest benefit to mitochondria in producing the energy needed to support these brain cells. Working in collaboration with the National Institute of Health Research (NIHR) Sheffield Biomedical Research Centre, the scientists will then move the molecules into a drug discovery phase.

“There is an urgent need for treatments to protect the nerve cells that become damaged in patients with Parkinson’s disease, which will have a crucial impact in slowing the progression of the condition and improving the quality of life” said Pamela Shaw, director of SITraN and and the university’s new Neuroscience Institute.

Potential treatments identified through this process will be further developed through a partnership with the NIHR Biomedical Research Centre at the Royal Hallamshire Hospital, a Sheffield teaching hospital, Shaw said, adding “[w]e are hugely grateful to Parkinson’s UK for supporting this important translational research.”

“We are delighted to partner and work with Dr Heather Mortiboys and her team at the University of Sheffield. Through our Virtual Biotech initiative, we are committed to accelerating promising and breakthrough treatments for Parkinson’s,” said Richard Morphy, drug discovery manager at Parkinson’s UK.

“This is an exciting new approach that could rescue defective mitochondria inside neurons to prevent dysfunction and degeneration of dopamine-producing brain cells,” Morphy said.

Parkinson’s UK, which invests about $4.8 million a year in work that advances potential treatments, estimates that about 148,000 people in the U.K. have this neurodegenerative disease.

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Researchers Contemplate Salivary Alpha-Synuclein as Parkinson’s Biomarker


Alpha-synuclein in saliva may be a potential biomarker for Parkinson’s disease, according to a recent review article, but more research is necessary to determine its reliability as a possible screening approach.

The study with that finding, “Salivary alpha‑synuclein as a biomarker for Parkinson’s disease: a systematic review,” was published in the Journal of Neural Transmission.

In Parkinson’s, a protein called alpha-synuclein clumps together, creating insoluble fibrils (small fibers) that accumulate inside nerve cells. These aggregates, known as Lewy bodies, are harmful to cells, eventually leading to cellular death, which then contributes to the onset of disease-related symptoms.

Unfortunately, alpha-synuclein aggregates can be confirmed only during an autopsy examination, so current diagnosis relies on Parkinson’s-related clinical symptoms instead of objective tissue changes.

That is why researchers are seeking reliable molecular biomarkers that can distinguish Parkinson’s from other conditions, monitor disease progression, or provide insight about a patient’s response to a given therapeutic intervention.

Lewy bodies have been found in the salivary glands of early-stage Parkinson’s patients. “Salivary alpha-synuclein is an easily accessible biomarker for PD [Parkinson’s disease] with promising results,” the researchers wrote.

The team decided to summarize the current knowledge of salivary alpha-synuclein as a potential biomarker for Parkinson’s. They searched the U.S. National Library of Medicine’s MEDLINE database from 1970 to April 2019 for several keywords related to Parkinson’s diseasem including “alpha synuclein,” “Lewy body pathology,” “saliva,” and “biomarker.”

Based on all their established criteria, researchers identified 476 studies, of which only eight had data on salivary alpha-synuclein, totaling 1,240 participants.

Of the eight studies, three reported total salivary alpha-synuclein levels (i.e., including all forms of the protein) were significantly lower in Parkinson’s patients, compared to healthy individuals, but the remaining five indicated no association between total alpha-synuclein concentration in saliva and the neurodegenerative disorder.

“In some studies, total salivary [alpha-synuclein] was associated with demographic and clinical features; however, no consistent pattern emerged. In one study, total [alpha-synuclein] levels were associated with poor cognitive performance in [Parkinson’s disease] patients,” the investigators noted.

Alpha-synuclein can be found in various molecular and structural forms. Half of the studies analyzed showed that people with Parkinson’s had higher levels of salivary oligomeric (aggregated) alpha-synuclein and a higher oligomeric alpha-synuclein/total alpha-synuclein ratio, than controls.

Additionally, one study indicated multiple genetic variants could alter total salivary alpha-synuclein concentrations in Parkinson’s. Nonetheless, in all studies there were important limitations to the scientific protocol and the corresponding results that may have influenced its conclusions. Some of those confounding factors included problems with sample collection, sample contamination, inadequate sample storage, or difficulties performing the tests.

“Utilization of saliva in biomarker discovery has several advantages over other biofluids. For instance, in comparison to CSF [cerebrospinal fluid, the liquid surrounding the brain and spinal cord] or serum/plasma, human saliva is readily accessible and is easier and less invasive to collect in adequate quantities,” the researchers explained.

Because of the minimal risk the approach imposes on the patient, salivary biomarkers may enable monitoring how the disease progresses and the effects of treatments.

Although studies suggest a decrease in total, and an increase in oligomeric,  salivary alpha-synuclein levels, results lack consistency. For now, salivary alpha-synuclein tests have yet to be adopted in clinical practice.

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Balance Issues Are Inevitable with Parkinson’s Disease


Years ago, Harrison Ford played the role of Henry Turner, the main character in the movie “Regarding Henry.”

Henry’s entire world shifts when he is shot in the head during a robbery at the convenience store where he was buying cigarettes. The nearly fatal injury puts him into cardiac arrest and he ends up with brain damage, specifically retrograde amnesia.

It takes several months for Henry to recover. When he is finally released from the hospital, he is not the man he used to be — an arrogant playboy who steps on others to get what he wants. The Henry from before was unfaithful to his wife, and his daughter was afraid of him. Henry post-injury is almost childlike, and upon learning who he was before the accident, tries to right some of his wrongs.

In the first few days home, Henry is sitting at the table with his daughter eating breakfast when she accidentally spills her milk on the kitchen table. Fear seizes her as she awaits Henry’s reaction. He sees the fear in her eyes, and to put her at ease, says, “It’s OK. I do that all the time.” He then tips over his glass of milk as well.

A few months ago, I read about a woman who had Parkinson’s disease (PD). She, like so many of us, was frequently dropping things, including her meals, which made her feel humiliated and embarrassed. Unfortunately, that’s what PD does. It gives you plenty of opportunities to be humiliated and embarrassed, always when you least expect it. But what we need to do is learn to go easy on ourselves. It’s not like we are doing these things on purpose.

The fact is that we all spill things, Parkinson’s or not. We all lose our balance and drop things or fall to the ground. Having PD just makes the opportunities more probable. We need to recognize that spills and falls are going to happen sooner or later, and we should try to be ready for it.

Here’s what you will need:

  • A cane or a walker
  • A helmet
  • Knee pads
  • Body armor
  • Elbow pads
  • Shin guards
  • Safety goggles
  • Leather gloves
  • Steel-toe boots
  • Brawny paper towels for those tough spills
  • Medic alert device to alert people that you have fallen and can’t get up
  • A sense of humor

A dog to lick up those spills wouldn’t be bad, either. Just decide that you are going to turn that 5-second rule into 20 — as we all know, things take just a little bit longer to do with PD!


Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

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Plant Antioxidant Seen to Aid Mitochondria and Ease Motor Problems in Early Parkinson’s Study

plants and antioxidants

Alpha-arbutin — an antioxidant found in plants such as blueberry bush — may restore mitochondrial function in nerve cells and ease the motor disabilities associated with Parkinson’s disease, according to a preclinical study from China.

Its results point to alpha-arbutin as a potential therapeutic compound for Parkinson’s and other disorders linked to problems in mitochondria, a cell’s energy source.

The study, “α-Arbutin Protects Against Parkinson’s Disease-Associated Mitochondrial Dysfunction In Vitro and In Vivo,” was published in the journal NeuroMolecular Medicine.

Parkinson’s disease is characterized by the degeneration and death of a specific group of nerve cells — called dopaminergic neurons —  in the substantia nigra, a region of the brain that regulates muscle movement and coordination. To work as intended, these nerve cells require large amounts of energy, which is provided by mitochondria.

Mitochondria are small organelles inside cells that, apart from being a cell’s “powerhouse,” are also the main producers of free radicals, or reactive oxygen species, which are associated with oxidative stress. Oxidative stress results from an imbalance between the production of free radicals and a cell’s ability to detoxify them, leading to cellular damage.

Increasing evidence suggests that both mitochondrial dysfunction and oxidative stress contribute to the degeneration of dopaminergic neurons seen in Parkinson’s disease. Compounds that can reduce mitochondrial dysfunction or oxidative stress may protect these neurons, and be potential therapies for Parkinson’s.

Alpha-arbutin, a natural compound extracted from plants of the heath family (Ericaceae) — which includes blueberry and bearberry bushes, and cranberry bogs — was shown to have antioxidative properties and to suppress the production of a key mediator of oxidative stress in Parkinson’s disease.

Researchers set out to evaluate the therapeutic potential of alpha-arbutin in two established preclinical disease models.

The first model involved nerve cells grown in the lab and treated with rotenone, a pesticide known to impair mitochondrial function, promote their production of free radicals, cause cellular death, and lead to parkinsonian features.

Giving alpha-arbutin to nerve cells before rotenone (pre-treatment) eased this pesticide’s toxic effects, suppressing free radical production and increasing the levels of antioxidative molecules. This worked to promote an oxidative balance, leading to fewer dead nerve cells.

Pre-treatment with alpha-arbutin also attenuated rotenone-induced mitochondrial damage to the cells and restored their ability to engage in autophagy, a vital cellular recycling system that removes or recycles unnecessary or dysfunctional components. Rotenone suppresses this natural process, damaging and killing cells.

These results suggested that alpha-arbutin’s neuroprotective effects were associated with a reduction in oxidative stress, and the maintenance of mitochondria function and autophagy processes.

Researchers then evaluated whether alpha-arbutin could ease Parkinson’s-associated symptoms and mitochondrial damage in fruit flies lacking the PRKN gene. Mutations in PRKN are known to trigger mitochondrial dysfunction, loss of dopaminergic neurons, and early-onset Parkinson’s disease.

Feeding these mutated flies alpha-arbutin significantly improved their climbing ability and wing posture, whose pre-treatment abnormalities are considered characteristic disease symptoms. The treatment also restored their mitochondrial structure and increased their energy production.

These findings, the researchers said, show for the first time that alpha-arbutin is able to not only significantly reduce rotenone-induced oxidative stress and mitochondrial dysfunction in nerve cells, but can also rescue motor problems and mitochondrial abnormalities in an animal model of Parkinson’s disease.

“Naturally derived-antioxidants might serve as a new class of therapeutic options for PD [Parkinson’s disease],” the researchers wrote.

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Low Vitamin D Levels Linked to Added Falls, More Sleep Problems, Depression, Study Shows

low Vitamin D

Low vitamin D levels are associated with a greater tendency for falls, sleep problems, anxiety, and depression in people with Parkinson’s disease, according to a recent study.

The findings, “Relationship between 25‐Hydroxyvitamin D, bone density, and Parkinson’s disease symptoms,” were published in the journal Acta Neurologica Scandinavia.

Vitamin D deficiency and low bone mass are frequently observed in people with Parkinson’s disease (PD). In fact, one particular study found that lack of this vitamin is more common in people with Parkinson’s (55% of patients) than other populations, such as people with Alzheimer’s disease (41% of patients).

But the relationship between vitamin D levels and Parkinson’s has remained controversial. Some studies suggest that taking vitamin D3 — a form of vitamin D used in supplements — can stabilize the disease, while others see no relation with the risk of Parkinson’s.

However, most studies have focused on limited aspects of the disease and did not include important outcomes — notably, non‐motor symptoms.

Vitamin D has a vital role in bone health, since it promotes calcium absorption and bone mineralization, which keeps bones strong and healthy. It also blocks the release of parathyroid hormone (PTH), an hormone that promotes bone tissue reabsorption and bone thinning.

Some studies support that lack of vitamin D results in a greater risk of falls and fractures in Parkinson’s patients, which can increase hospitalization and even fatal disability. Its levels also have been associated with cognition and mood, as well as stomach malfunction, in people with the disease.

While it is possible that deficits in this vitamin impact several symptoms of PD, the connection remains unclear.

To shed light on this relationship, researchers at the Second Affiliated Hospital of Soochow University and Soochow University, in China, set out to determine if vitamin D levels correlated with bone mineral density (BMD) and non‐motor symptoms in Parkinson’s patients.

The team measured blood levels of 25-hydroxyvitamin D, or 25(OH)D — a precursor of the active form of vitamin D and the most accurate indicator of vitamin D levels in the body — and performed extensive clinical evaluations in 182 Parkinson’s patients as well as 185 healthy people (controls).

Participants were recruited from the Second Affiliated Hospital of Soochow University from March 2014 to December 2017.

Bone mineral density — a measure of bone mass and health — was measured at the lumbar spine and the top of the femur (thigh bone) by bone densiometry, which measures bone loss.

The data showed that people with Parkinson’s had significantly lower vitamin D levels in the blood compared with healthy controls — an average of 49.75 versus 43.40 nanomol per liter of 25(OH)D.

In agreement, low levels of vitamin D (below 50 nmol/l) also were more common in Parkinson’s patients (68.68%) than controls (54.05%).

People with lower vitamin D levels were more likely to fall and experience sleep problems, including difficulty in falling asleep (insomnia). They also had significantly more depression and anxiety.

Mean bone densities in both the spine and femur were lower in PD patients, however no correlation was seen between the levels of BMD and vitamin D.

“Together, these results indicate that vitamin D deficiency may play a role in PD pathogenesis [disease manifestations], while vitamin D supplementation may be used to treat the non‐motor symptoms of PD,” the researchers  said.

“As various non-motor symptoms place a burden on individuals with Parkinson’s disease and their caregivers, vitamin D might be a potential add-on therapy for improving these neglected symptoms,” study’s senior author Chun Feng Liu, MD, PhD, said in a press release.

However, the researchers stressed that future studies with a larger sample size are necessary to clarify the role of vitamin D in Parkinson’s disease.

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