Could this brain stimulation technique reverse memory decline?

April 18, 2019      By Ana Sandoiu

New research suggests that transcranial magnetic stimulation could reverse age-related memory loss. In fact, the technique restored the memory of senior participants to the level of young adults.

It is a known fact that a person's memory tends to decline with age. Between 15 and 20 percentof people over the age of 65 years have mild cognitive impairment (MCI) — a condition that is no cause for concern on its own but that raises the risk of Alzheimer's disease.

Misplacing things once in a while or having trouble finding one's words can be a natural partof the aging process. However, researchers may now have found a way to reverse this form of age-related memory loss.

Joel Voss, who is an associate professor at the Northwestern University Feinberg School of Medicine in Chicago, IL, is the lead investigator of the new study.

Voss and his team used a noninvasive form of brain stimulation called transcranial magnetic stimulation (TMS) to improve memory in older adults. The researchers published their findings in the journal Neurology.

Using TMS to target the hippocampus

TMS works by applying magnetic fields to specific brain areas, thus affecting the central nervous system. The technique operates completely outside of the body, which means that it is noninvasive.

In this case, Voss and team applied TMS to the participants' hippocampus — a brain area that shrinks with age and that previous research has linked with age-related memory loss.

The hippocampus is "the part of the brain that links two unrelated things together into a memory, like the place you left your keys or your new neighbor's name," explains the lead researcher. "Older adults often complain about having trouble with this."

In the current study, Voss and team recruited 16 adults aged between 64 and 80 years and used functional MRI to locate the hippocampus in each participant.

As the hippocampus is too deep in the brain for the magnetic fields to reach it, the researchers targeted a superficial brain area in the parietal lobe that connects with the hippocampus instead. Doing this made it possible to use TMS to affect the hippocampus indirectly.

"We stimulated where brain activity is synchronized to the hippocampus, suggesting that these regions talk to each other," explains Aneesha Nilakantan, the study's first author.

The researchers applied high-frequency magnetic stimulation to this brain area for 20 minutes each day for 5 consecutive days. Before and after the intervention, the researchers tested each participant's memory using standard memory tests.

The tests involved remembering random associations between a variety of things, such as objects, places, or words. Usually, young adults get 55 percent of these associations correct while older adults score below 40 percent.

Memory restored to young adult level

After receiving the TMS intervention, the seniors in the study scored the same as young adults typically would in the standardized memory tests.

Voss and team also carried out a sham intervention, which did not yield the same results

Older people's memory got better up to the level that we could no longer tell the apart from younger people. They got substantially better." Joel Voss 

The lead researcher comments on the uniqueness of the study, saying, "There is no previous evidence that the specific memory impairments and brain dysfunction seen in older adults can be rescued using brain stimulation or any other method."

In the near future, the researchers plan to test this approach in people with MCI.

https://www.medicalnewstoday.com/articles/325010.php?utm_source=newsletter&utm_medium=email&utm_country=US&utm_hcp=no&utm_campaign=MNT%20Daily%20Full%20%28non-HCP%20US%29%20-%20OLD%20STYLE%202019-04-18&utm_term=MNT%20Daily%20News%20%28non-HCP%20US%29

Drug used to treat high blood pressure could relieve Parkinson's, Huntington's and Alzheimer's by encouraging 'Pac-Man-like cells to eat away toxic protein build-ups in the brain'

By ALEXANDRA THOMPSON SENIOR HEALTH REPORTER   April 18, 2019

• Felodipine reduced the build-up of proteins in the brains of mice and zebrafish 
• Triggered 'defective cells' to 'eat themselves', with the waste then broken down
• Drug dose required in mice was lower than expected, suggesting it is safe 

A drug that is used to treat high blood pressure may relieve Parkinson's, Huntington's and Alzheimer's, research suggests.  

A study found felodipine reduced the toxic build-up of proteins in the brains of mice and zebrafish with neurodegenerative diseases.

Felodipine triggered the animals' 'defective cells' to undergo autophagy, when cells 'eat' themselves like 'Pac-Man', with the leftover waste being broken down.

Autophagy occurs naturally in healthy people but is impaired in those with diseases such as Alzheimer's.

The drug dose required was also lower than anticipated, prompting the University of Cambridge researchers to be 'cautiously optimistic' about their findings.

A drug that is used to treat high blood pressure may relieve Parkinson's, Huntington's and Alzheimer's. It works by triggering' 'defective cells' to undergo autophagy. This occurs when cells 'eat' themselves like 'Pac-Man' (pictured), with the leftover waste being broken down

The team was led by Professor David Rubinsztein, deputy director of the Cambridge Institute for Medical Research and professor of molecular neurogenetics.  

'This is the first time that we're aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans,' he said.

'As a result, the drug was able to slow down progression of these potentially devastating conditions and so we believe it should be trialled in patients.'

Professor Rubinsztein added: 'This is only the first stage, though.The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice. 

'We need to be cautious, but I would like to say we can be cautiously optimistic.'

Parkinson's, Huntington's and dementia are all examples of neurodegenerative diseases. 

These occur when neurones - cells that carry signals to and from the brain - lose their function over time and ultimately die. 

A common feature of these conditions is misfolded proteins, such as huntingtin in Huntington's disease and tau in some forms of dementia, the authors wrote in the journal Nature Communications. 

A study found felodipine reduced the toxic build-up of proteins in the brains of mice and zebrafish with neurodegenerative diseases (stock)

The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice. 

'We need to be cautious, but I would like to say we can be cautiously optimistic.'

Parkinson's, Huntington's and dementia are all examples of neurodegenerative diseases. 

These occur when neurones - cells that carry signals to and from the brain - lose their function over time and ultimately die. 

A common feature of these conditions is misfolded proteins, such as huntingtin in Huntington's disease and tau in some forms of dementia, the authors wrote in the journal Nature Communications. 

hese proteins accumulate to cause irreversible damage to brain cells. And patients with neurodegenerative diseases are unable to clear these proteins due to their autophagy process being impaired.

HOW TO DETECT ALZHEIMER'S

Alzheimer's disease is a progressive brain disorder that slowly destroys memory, thinking skills and the ability to perform simple tasks.

It is the cause of 60 percent to 70 percent of cases of dementia.

The majority of people with Alzheimer's are age 65 and older.

More than five million Americans have Alzheimer’s.

It is unknown what causes Alzheimer's. Those who have the APOE gene are more likely to develop late-onset Alzheimer's.

 Signs and symptoms:

• Difficulty remembering newly learned information
• Disorientation
• Mood and behavioral changes
• Suspicion about family, friends and professional caregivers
• More serious memory loss
• Difficulty with speaking, swallowing and walking

Stages of Alzheimer's:

• Mild Alzheimer's (early-stage) - A person may be able to function independently but is having memory lapses
• Moderate Alzheimer's (middle-stage) - Typically the longest stage, the person may confuse words, get frustrated or angry, or have sudden behavioral changes
• Severe Alzheimer's disease (late-stage) - In the final stage, individuals lose the ability to respond to their environment, carry on a conversation and, eventually, control movement

There is no known cure for Alzheimer's, but experts suggest physical exercise, social interaction and adding brain boosting omega-3 fats to your diet to prevent or slowdown the onset of symptoms.

And in the UK, 850,000 people have dementia, with Alzheimer's being the most common type of the disease, Alzheimer's Society says. And around 145,500 people are living with Parkinson's, according to Parkinson's UK.

Neurodegenerative diseases are set to rise as the global population ages, with effective drugs needed more now than ever, the researchers wrote.

However, no medication successfully induces this 'Pac-Man' effect - as described by the researchers - in these patients. 

When looking for new drugs, scientists often experiment with existing ones due to them already being known to be safe in humans. 

Inspired by past studies that found a link between hypertension drug felodipine and a reduced risk of Parkinson's, the researchers gave the medication to mice that had been genetically modified to express mutations that cause Huntington's and Parkinson's.

Mice were chosen due to their short life span and fast reproductive rate, which enables scientists to quickly investigate the biological impact of a drug. 

And aspects of the rodents' physiology share similar characteristics with humans, such as their nervous system.

The scientists also gave felodipine to zebrafish with a form of dementia.

Results revealed both animals showed reduced signs of their respective diseases following treatment. 

Although mice studies typically use doses that are much higher than what is considered safe for humans, the researchers saw even low levels of the drug led to benefits for the rodents with Parkinson's.

They controlled the concentration of the drug being administered via a small pump beneath the mice's skin. 

Fiona Carragher, chief policy and research officer at Alzheimer's Society - which partially funded the study - added: 'With no new treatments for dementia in over 15 years, it's encouraging to see that re-purposing an existing drug has showed signs of reducing key hallmarks of some types of dementia. 

'However, it's still early days and more research is needed to fully understand this drug's potential in tackling the symptoms of the condition and to examine dosage and side effects.' 

https://www.dailymail.co.uk/health/article-6935481/Drug-used-treat-high-blood-pressure-relieve-Parkinsons-Huntingtons-Alzheimers.html?ns_mchannel=rss&ito=1490&ns_campaign=1490

25th Parkinson's Unity Walk to Take Place on Saturday, April 27th in New York City's Central Park

April 17, 2019

KINGSTON, New Jersey (WABC) -- Let's walk together, in the largest grassroots fundraiser for Parkinson's disease research in the United States! 

The Parkinson Alliance announced today that the 25th Parkinson's Unity Walk will take place on Saturday, April 27, 2019, at 8:30 am in New York City's Central Park to raise funds and unite the community in the battle to eradicate Parkinson's disease. 

Thousands of participants including patients, caregivers, family, and friends, are expected to gather in the largest single-day grassroots fundraiser for Parkinson's disease research in the United States. 

Since the Unity Walk's inception in 1994, $25 million in donations have been raised, 100% of which has funded hundreds of research studies, taking us steps closer to finding a cure for Parkinson's disease. This was the vision of the founder of Parkinson's Unity Walk, Margot Zobel, 25 years ago, when Margot, with the help of 200 friends, family members, and fellow patients held the first walk, raising $16,000 for research. For 25 years, the Unity Walk has continued to grow in participation and impact, with over 11,000 participants walking together at last year's event. 

Martin Tuchman, Chairman of The Parkinson Alliance, stated that "Last year the Unity Walk raised over $1.5 million and while every penny of that is now funding vital research, until we find a cure, we must continue walking and funding research. Parkinson's disease is a chronic, degenerative, neurological disorder that affects at least one million people in the United States. Sixty thousand new cases (one person every nine minutes) are diagnosed each year, and we need continuing research to keep advancing our progress." 

In addition to the 1.4-mile wheelchair accessible walk route, participants will have opportunities to meet with healthcare experts and learn more about nationally recognized Parkinson's disease exercise programs, and movement disorders centers. Carol Walton, Executive Director of the Parkinson's Unity Walk, explained that "There are many reasons to walk with us. The Unity Walk is more than a fundraiser; it is a gathering for the community to meet and be inspired by other members in the Parkinson's community. Visit with our sponsors to learn about current medical therapies and learn about the support that's available for them." Walton added that "In addition to our sponsor and Parkinson's disease informational booths, festivities include our Make-a-Sign and Kids' Booth." 

With the backing of our supporters, we have funded hundreds of studies since the Unity Walk's inception in 1994. We are proud to partner with our sponsors. Because of their support, every donation goes directly to help fund Parkinson's disease research for four leading organizations: American Parkinson Disease Association, Parkinson's Foundation, The Michael J. Fox Foundation for Parkinson's Research, and The Parkinson Alliance. Sunovion Pharmaceuticals Inc. is the Premier Sponsor for the 2019 Parkinson's Unity Walk. Additional sponsors include US WorldMeds, Abbott, Adamas, Lundbeck, UCB, AbbVie, Acorda, Amneal, Boston Scientific, Kyowa Kirin, LSVT Global, Medtronic, Vertical Pharmaceuticals and Voyager Therapeutics. 

Please join us on Saturday, April 27th in New York City's Central Park for the 25th Parkinson's Unity Walk. The Walk's rolling start begins at 8:30 am. Registration, and Sponsor and Informational Booths are also open at 8:30 am. For information, please visit our website at unitywalk.org or call (866) 789-9255. 

For information about how to join the 2018 Parkinson's Unity Walk, visit unitywalk.org or call (866) 789-9255. 

--- 

About The Parkinson Alliance 

The mission of The Parkinson Alliance is to raise funds for research to end Parkinson's disease, support the development of new therapies, and improve the quality of life for those living with the disease through patient-centered research and resources. The Parkinson Alliance stands as an umbrella organization for the Unity Walk, Team Parkinson, and other fundraising events held around the country. Taken together, we have funded nearly $30 million in research since our founding. 

https://abc7ny.com/society/25th-parkinsons-unity-walk-to-take-place-on-saturday-april-27th-in-new-york-citys-central-park/3210002/

Stimulating brain with ultrasound can influence decisions

Wednesday 17 April 2019 By Catharine Paddock PhD

A noninvasive, low-intensity ultrasound method that targets nerve cells, or neurons, can alter brain function to influence decision-making.

New research shows how a brain area called the anterior cingulate cortex controls a type of reasoning known as counterfactual thinking. 

Scientists have demonstrated the technique in a recent study, in which they disrupted "counterfactual thinking" in primates.

Counterfactual thinking, or counterfactual reasoning, is a type of decision-making that involves considering options that are not available now but could be in the future.

For example, a person working indoors on a sunny day who says to themselves, "I could be outside enjoying the sunshine," is engaging in counterfactual thinking.

The recent study is the first to show that a frontal brain region known as the anterior cingulate cortex can regulate counterfactual thinking.

In a paper in Nature Neuroscience, the authors describe how they altered counterfactual thinking in macaque monkeys by targeting neurons in their anterior cingulate cortex with noninvasive, low-intensity ultrasound.

'Internal representations of choices'

Research on decision-making has tended to focus on brain circuits that control responses to current stimuli. However, the authors note that "Animals often pursue behaviors for which there is currently no sensory evidence."

They argue that, to be able to do this, animals have to maintain "internal representations" of choices, "even when these choices are unavailable."

In other words, animals must have some capacity for counterfactual thinking, or thinking about choices that are unrelated to current experience.

"This is a really exciting study for two main reasons," says lead and corresponding study author Elsa Fouragnan, Ph.D., who works at the University of Plymouth School of Psychology, in the United Kingdom.

The first reason for being excited by the study, she explains, is because the findings reveal that "the cingulate cortex is crucial to help switch to better alternatives."

And the second reason, she adds, is because the results show that "low-intensity ultrasound can be used to reversibly change brain activity in [a] very precise part of the brain."

Nonsurgical brain stimulation

There is a growing need for nonsurgical brain stimulation tools. There is potential for such methods to improve treatment outcomes safely and with minimum side effects.

Low-intensity, focused ultrasound is "gaining traction" as such an approach. Previous studies have shown that it can alter activity in mammal brains noninvasively, both by stimulating and blocking signals.

Some studies have also shown that ultrasound can influence activity in the outer layers and also deep inside the human brain.

The recent study sheds light on how activity in the anterior cingulate cortex influences decision-making.

It suggests that, if this part of the brain does not function properly, it could prevent an individual from being able to switch to a better option, even when it becomes available.

Experts believe that this type of brain dysfunction could be the reason why people with certain psychiatric illnesses remain trapped in unhelpful habits.

Study reveals causal role of brain region

Fouragnan and colleagues investigated these possibilities further by studying the macaques as they searched for and selected a treat from a range of options.

The monkeys rapidly learned which of the options they preferred, but when it came to exercising choice, it was not always available. However, they did "keep it in mind" for when it was next available.

The researchers then investigated how the monkeys "maintained representations of the value of counterfactual choices – choices that could not be taken at the current moment but which could be taken in the future."

Using MRI scans of the monkeys' brains, they observed that activity in the cingulate cortex "reflected whether the internal value representations would be translated into actual behavioral change."

They showed that, by stimulating the brain region with noninvasive, focused, low-intensity ultrasound, the anterior cingulate cortex was of "causal importance" to this process. Stimulating the brain in this way disrupted the monkeys' counterfactual thinking.

Fouragnan concludes that brain stimulation using noninvasive, focused, low-intensity ultrasound "has the potential to improve the lives of millions of patients with mental health conditions by stimulating brain tissues with millimeter accuracy."

Some brain stimulation techniques are already helping people with Parkinson's disease and depression, but because they are nonsurgical, the methods do not have the level of accuracy achieved in this study, she adds.

"It's still early stages, and the next stage is for further trials to be conducted in humans, but the potential is very exciting."

Elsa Fouragnan, Ph.D.

https://www.medicalnewstoday.com/articles/324998.php

Sidekicks' Event To Bring Together Kids, Parkinson's Patients

By Lisa Marie Farver, Patch Staff | Apr 17, 2019 

Glen Ellyn is one of 10 locations throughout the U.S. to host the Sidekicks event, which brings together kids and Parkinson's patients. 

GLEN ELLYN, IL -- Glen Ellyn is gearing up to be just one of the first places to host a special event that brings together young children and adults patients with Parkinson's Disease. The Sidekicks event, slated for April 26 and 27, will feature interactive art sessions between kids and patients, along with a formal art showcase that will help bring awareness to the challenges of living with Parkinson's. 

During the Sidekicks art sessions, kids and Parkinson's patients will decorate friendship rocks, bring "Ideascapes" to life, and share stories with "Storyprints," a form of handprint art. Sidekicks is sponsored by the Lundbeck and The Davis Phinney Foundation. 

In a news release, Kayla Ferguson, Sidekicks Program Manager at the Davis Phinney Foundation, said, "With Sidekicks, people with Parkinson's and their youth partners can thrive by working together to gain information and insights into one another's experiences. It's a lot of fun and creates memorable moments of victory for participants."

"There is a common feeling of isolation among people with Parkinson's," said Charise Dunn, Senior Manager of Advocacy and Patient Support at Lundbeck. 

She added that "Sidekicks is a great example of our commitment to partnerships and programs focused on creating community connections and supporting overall brain health so every person can 

What: Sidekicks Program and Showcase 

When: April 27: Art showcase at 12:30 p.m. 

Where: Glen Ellyn Police Department, 65 S. Park Blvd., Glen Ellyn 

https://patch.com/illinois/glenellyn/sidekicks-event-bring-together-kids-parkinsons-patients

Epigenetic study reveals potential for earlier diagnosis in Parkinson’s disease

April 17, 2019     Gabrielle Hirneise

Parkinson's disease originates from the loss of neurons releasing dopamine. Because these neurons control coordination in movement, their loss results in a multitude of movement-related deficiencies.

Parkinson’s disease, a neurodegenerative disorder, largely affects movement and causes irreversible neuronal damage. It may start with a tremor or it may be manifested in a speech problem; however, by the time symptoms are evident, it is too late to halt the course of the disease. 

Parkinson's originates from the loss of neurons releasing dopamine. Because these neurons control coordination in movement, their loss results in a multitude of movement-related deficiencies.

Although there is medication to treat the symptoms of Parkinson's, there is no known cure. To mediate this problem and propose more effective therapeutic strategies, an earlier diagnosis is key. 

“One of the biggest issues with neurodegenerative diseases like Parkinson’s disease or Alzheimer’s disease is that diagnosis is mostly clinically based, and it comes late in the disease — the brain is already degenerated, and it is extremely difficult to restore brain function at that stage,” said Travis Dunckley, an assistant research professor at the ASU-Banner Neurodegenerative Disease Research Center and the School of Life Sciences.

Dunckley teamed up with other universities including UCSD, Texas A&M and Harvard University and research institutes such as TGen to study the epigenetic changes in Parkinson's patients over time, specifically alterations in DNA methylation patterns over the course of the disease. If researchers were to obtain a better understanding of the DNA methylome in Parkinson's patients, they could potentially diagnose the disease earlier.

Currently, the disease is identified through clinical symptoms related to physical movement.

“When physicians treat PD patients, it is usually too late to change the trajectory of the disease. I am interested in early diagnostics to try to identify people prone to the disease before they get it,” Dunckley added. “Using this approach, you could put patients at risk for PD on certain therapies before symptoms arise.”

Parkinson's is governed both by genetic factors and environmental factors, making epigenetics an apt area of study.

“It’s about 60% environmental — it’s much less genetic than many other neurodegenerative diseases,” Dunckley said. “It’s made of up of environmental interactions with the genome. One of the major ways that the environment acts with the genome is through epigenetics.”

DNA methylation, one form of epigenetic alteration of genes, is a process during which methyl groups are added to DNA. These methyl groups can change the activity of the DNA without changing its sequence. However, in the context of Parkinson's disease, it can be difficult to conclude that changes in DNA methylation are solely correlated to disease progression.

“It is hard to link them without confounding variables in that there are a lot of environmental factors,” Dunckley said. “It’s difficult to say whether epigenetic changes are based on disease, environmental factors or a combination of disease and environmental factors.”

In this study, the largest longitudinal epigenetic study in Parkinson's disease to date, 189 patients’ methylomes were studied and compared to that of 191 control subjects. Two years later, their methylomes were compared once again.

The project identified distinct methylation patterns in Parkinson's patients relative to control patients and identified specific sites at which methylation changed longitudinally. The study also found differences in methylation patterns for those subjected to anti-Parkinson’s drugs (dopamine replacement drugs) versus those who received no treatment. The researchers found that DNA methylation changed more for those patients without treatment, further exacerbating the link between epigenetics and Parkinson's progression.

“The main findings are that one, the epigenome does change as the disease progresses. The second finding is that the PD medications themselves alter the epigenome,” Dunckley added. 

If researchers can identify changes in methylation that are characteristic of Parkinson's disease, they can diagnose earlier, allowing for more effective therapeutic strategies before there is irreversible damage. The methylation signatures are therefore promising candidates for biomarkers useful in early detection. 

To expand the scope of the project, Dunckley and his counterparts are repeating the same study but with a longer range of time and with a new subset of patients. 

“The next study we are doing is a replication and extension of this one to validate the findings and extend the observation period to five years,” Dunckley said. “We are also including patients that are very early in PD progression, patients who have symptoms that are highly predictive of future PD. The ultimate goal is to identify changes in these earliest stages of disease that can be predictive of future PD onset.”

Further exploration of epigenetic changes like DNA methylation promise to expand the understanding of this enigmatic disease and hopefully point the way to effective treatments.

https://asunow.asu.edu/20190417-discoveries-epigenetic-study-reveals-potential-earlier-diagnosis-parkinsons-disease

I’m Excited About the Potential of the PKG-Watch for Parkinson’s Care

 APRIL 17, 2019 BY "SHERRI WOODBRIDGE."

While at my boxing class the other evening, one of my classmates told me about a watch he is testing. It is called the Personal KinetiGraph (PKG)-Watch. This device is not to be confused with the Emma Watch, which was designed by a Microsoft inventor for Emma Lawton, a young British woman with Parkinson’s disease, to ease tremors in her hands.

There was considerable interest in the Emma Watch within the Parkinson’s community at the time the invention was announced in late 2017. A project to develop a device based on the watch is ongoing.

Enter the PKG-Watch

The PKG-Watch continuously collects data, including the movement symptoms of tremor, bradykinesia, and dyskinesia, as well as their severity and timing, while the wearer is engaged in daily activities. It also can be programmed to remind a patient to record that they’ve taken their Parkinson’s disease medication, according to Dr. Dominic Paviour, a European neurologist who has been testing it with his patients. 

“The PKG™ helped me to understand what [a patient’s] typical day was like and helped me to make some medication changes to improve his symptoms,” Paviour said, according to a story on the site Parkinson’s Life. “While the PKG™ is not telling us which medical adjustments to try, it is another piece of data that guides our decision-making process.”

My boxing buddy knew that I was interested in the watch, so he brought it to class and gave me the brochure that came with it to read.

The following is information I gleaned from the brochure and the website of the manufacturer, Global Kinetics:

Your doctor will refer you for a PKG-Watch. You wear it on your wrist for seven days. At the end of the week, you return the watch, and the results are sent to your doctor. These data show them how your movement changed throughout the day.

The watch can also be programmed to vibrate to remind you when it’s time to take your medications.

One of the significant benefits of this watch is that the data it collects can help your doctor to make better decisions about the type, dosage, and timing of medications.

I think the PKG-Watch is fascinating and I’m looking forward to finding out how it can improve Parkinson’s care.

***

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.

https://parkinsonsnewstoday.com/2019/04/17/pkg-watch-movements-tremors-medication/