Useful Fitness and Informational Resources for Parkinson’s Patients

More than 10 million people are living with Parkinson’s disease around the world. While this number seems shocking, it also means that we have a lot of people fighting for change, relief, a cure, or a solution to some of the difficulties that Parkinson’s yields. Research and interest in Parkinson’s are making connections easier, and more and more gyms are offering Parkinson’s fitness programs. Whether you’re looking for fitness resources, a good book or blog, or educational platforms, the following internet links might offer some inspiration.


Fitness resources

Exercise is healthy for everyone, but there’s evidence that it helps Parkinson’s patients manage certain symptoms of the disease. Parkinson’s specific exercise classes are popping up all across the country. How do you find a group that fits your interests? What if you don’t have access to a Rock Steady Boxing location? Or what if boxing isn’t the right fit for you?


Adaptive Training Foundation

The Adaptive Training Foundation aims to empower its participants through high-intensity athletics and community building. Its programs — Redefine, Reignite, Redeploy — help adaptive athletes push themselves to new levels of fitness, compete successfully, and challenge themselves physically. The facility is located in Texas.


PD Movement Lab (New York)

Pamela Quinn opened the first PD Movement Lab in 2006 to explore Parkinson’s through dance. A patient herself, Quinn uses her background in dance to experiment with a variety of techniques in order to help her students find solutions to mobility issues. PD Movement Lab is a New York company with branches in Manhattan and Brooklyn, but the organization is expanding its online presence to make dance accessible to anyone with Parkinson’s.


Parkinson’s Cycling Coach

There’s evidence that pedaling really fast can help reduce Parkinson’s symptoms by up to 35 percent. The people at Parkinson’s Cycling Coach aim to train people to lead indoor cycling classes, which will help patients benefit year-round. Cycling can be done at home or with a group, indoors or outdoors. And if you’re looking for a goal, Pedaling 4 Parkinson’s is an annual race that takes place in Colorado. The proceeds are donated entirely to Parkinson’s research. Having an event to train for might give you a bit of inspiration.


Informational resources

As Parkinson’s progresses, it becomes more difficult to leave the house. Physical developments make transportation tricky, and sometimes you just don’t want to be seen struggling. Resources are out there. Whether you’re seeking information or a way to exercise on your own, the internet is full of incredible platforms.


American Parkinson Disease Association

The American Parkinson Disease Association (APDA) is a grassroots organization dedicated to fighting Parkinson’s by way of fundraising, education, and public elevation. ADPA provides current news that’s related to developments in the disease and offers a location finder to help you get in touch with Parkinson’s resources near you. Its website includes information that’s tailored to specialized communities, like veterans, first responders, bilingual patients, and early-onset patients (those diagnosed before the age of 50).


Stanford Medicine

Stanford Medicine, in partnership with APDA, has an incredible community outreach webpage. It includes information on local support groups and exercise classes, and offers resources like fact sheets, books, exercise videos, and live-streaming fitness classes for a wider internet audience. The “Living with PD” category touches on topics like the effect of Parkinson’s on driving ability and shares the stories of individuals’ experiences with deep brain stimulation surgery. This is a terrific resource for those who want credible information about Parkinson’s.


The right stuff

Navigating change can easily become overwhelming, and everyone’s experience with the progression of Parkinson’s is different. This can make it hard to find resources that are relevant to your situation. With a click of the mouse, however, you can access a range of information sources and fitness programs that might help you manage your disease. These websites are good places to start.


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.



Young - Onset Parkinson's Disease

About 10 to 20 percent of people with Parkinson's experience symptoms before age 50, which is called "young onset." While treatments are the same, younger people may experience the disease differently. Scientists are working to understand the causes behind young-onset Parkinson's.


People with young-onset Parkinson's disease (YOPD) may have a longer journey to diagnosis, sometimes seeing multiple doctors and undergoing several tests before reaching a correct conclusion. As with Parkinson's diagnosed later in life, YOPD is diagnosed based on a person's medical history and physical examination. When younger people and their clinicians are not expecting Parkinson's disease (PD), the diagnosis may be missed or delayed. It's not uncommon for arm or shoulder stiffness to be attributed to arthritis or sports injuries before Parkinson's is eventually diagnosed.


In everyone with Parkinson's, both genetic changes and environmental factors likely contribute, to different degrees, to cause the disease. In younger people, especially those who have multiple family members with Parkinson's, genetics may play a larger role. Certain genetic mutations (in the PRKN gene, for example) are associated with an increased risk of young-onset PD. If you have YOPD (and particularly if you have a family history of Parkinson's), you may consider genetic testing to see if you carry one of these mutations. Testing can be done through your doctor's office but mainly is done in clinical studies since results currently don't change the medications you take. As part of research, genetic information offers valuable insights toward better understanding of the disease and potential therapies. Discuss the pros and cons with your family, your doctor and a genetic counselor.

Symptoms and Progression

People with YOPD are more likely to experience dystonia — prolonged muscle contractions that lead to abnormal postures, such as twisting of the foot. Also, younger people are more likely to develop dyskinesia — involuntary, uncontrolled movements, often writhing or wriggling — as a complication of long-term levodopa use combined with a long course of Parkinson's disease.

On the other hand, people with YOPD are less likely to have significant problems with balance, or considerable memory or thinking problems (dementia). Progression of disease over time is, in general, slower.

Treatment Options

Options for managing Parkinson's symptoms are essentially the same no matter when Parkinson's is diagnosed. To delay dyskinesia, younger people may choose to postpone starting medication or begin with Parkinson's drugs other than levodopa, especially if symptoms are mild and don't interfere with work, physical or social activities. Options may be to start with an MAO-B inhibitor; amantadine; a dopamine agonist; or, when tremor is particularly prominent, an anticholinergic drug.

Physicians and researchers have long engaged in a healthy discussion over the best time to start levodopa. Some believe it's better to start sooner to control symptoms, maximize quality of life and allow a person to remain active as long as possible. Others hold off to potentially delay motor complications, such as dyskinesia. Ask your physician for his or her take on this issue and consider the pros and cons of both approaches. Work closely with your movement disorder specialist to determine which medication is right for you and when.

Research into Young-onset

Scientists are studying the genetic connections to young-onset Parkinson's disease, such as mutations in the PRKN gene, and other contributing factors. That information could lead to preventive strategies and treatments. Researchers also are working diligently — often with funding and/or leadership from The Michael J. Fox Foundation (MJFF) — to develop objective tests for Parkinson's so the path to a confirmed diagnosis won't be as long.

While participating in a clinical trial may be the furthest thing from one's mind when processing a YOPD diagnosis, many studies of therapies to slow or stop progression need people who were recently diagnosed and have not begun medication. Learn more about recruiting studies on our Fox Trial Finder matching tool and talk to your doctor about enrolling in trials.

Young-onset Considerations

Although everyone with Parkinson's wonders what the years ahead hold, this may be top of mind in those who have a longer future with PD. Concerns often center on the potential implications of the disease on personal, family and professional desires and responsibilities.

support group of other people with young-onset Parkinson's disease may help you address some of these challenges. A local or national Parkinson's organization or your physician may be able to refer you to a YOPD group — either in-person or online. If you haven't found a group that fits your needs, consider starting your own.


Depending on what symptoms you have, how significant they are and what you do for a living, you may be able to continue working for a significant period of time beyond diagnosis. (Many people do.) Still, having a backup plan, including schedule changes, early retirement or even a different career, may be worthwhile. Whether and when to disclose your diagnosis to coworkers and employers are personal decisions. Having a strategy that outlines who you'll tell, how you'll guide the conversation and how you'll handle potential reactions can be helpful. Find practical tips and tools in our two-part guide:

You also may want to familiarize yourself with the Americans with Disabilities Act (ADA) in case you need to seek accommodations under these guidelines.


Financial planning may take on a new light with your diagnosis. You may want to take a fresh look at your current financial status, factoring in debt and savings and thinking about the need for regular doctors' visits and medications. It's a good idea to map out future financial goals and reevaluate life insurance coverage. Explore disability and long-term care insurance options, even though they may never become necessary.

Family Planning

Although the data on pregnancy and PD is limited, plenty of women with Parkinson's disease have successfully carried healthy babies to term. Taking birth control pills does not mean you cannot take Parkinson's drugs, but doses may need to be adjusted. Couples living with Parkinson's might therefore wish to consider other forms of contraception.


Parents may worry about caring — physically and financially — for young children, whether their children are at increased risk of developing the disease, and how to tell them about the diagnosis. Parents in the MJFF community have found it helpful to convey the facts using words directed to the child's level of education, express optimism where possible and offer reassurance. Sometimes engaging in family activities around Parkinson's is comforting — for example, looking up answers to a child's questions together, brainstorming a school project around the topic of PD or fundraising to support research.

Motor and non-motor symptoms may pose logistical challenges when raising children. It may be useful to establish a group of family, friends and neighbors who can help when necessary — such as with babysitting or carpooling — and think about restructuring household roles and responsibilities.

People in midlife may find parenting issues compounded if they are part of the "sandwich generation," caring for or supporting their own parents as well as their children. Social workers can be a good resource to lay out options for these situations.

Relationships and Marriage

Parkinson's can impact relationships with significant others and spouses. Talking openly and honestly about present and future concerns, as well as addressing symptoms and issues related to sexual health as they arise, can be helpful. Cooperation and flexibility — important in any partnership — become even more critical when managing life with Parkinson's together.



Positive Things to Say to PD Patients

Why is it important for someone with Parkinson’s disease to hear something positive said to them? There is enough negativity around us, be it environmental, political, domestic or international, those of us living day-to-day with a health condition can use a reminder of the positive stuff. Words have real power!

When I decided to write about what to say to someone with Parkinson’s that’s positive, I failed to ask whether the person that I was talking to was newly diagnosed or may have had it for a while. Having had this illness since the age of 17 and diagnosed at the age of 23, my perspective comes from learning to live well with Parkinson’s disease for three decades. I will add that a great deal of my early years with Parkinson’s came out of trial and error and experimenting to see what I found benefit from and what I didn’t.

The following list contains what every person with Parkinson’s needs to know whether they are newly diagnosed or have had it longer than me. I hope that you agree that these are vital messages to share throughout our community:


You are NOT alone!

Try not to be overwhelmed by your diagnosis. Like all of us, our future is unknown and undetermined. Take the best possible care of yourself that you can.

There’s help and information available to you that wasn’t out there when I was diagnosed, so long ago. The network of people, resources, knowledge, compassion, and medical expertise spread amongst this planet is truly inspiring and amazing! The Parkinson’s community is a close-knit group of dedicated individuals, organizations, and foundations, offering support, research, and various programs that may show benefit to your condition! Read the various informative blogs, news feeds, and daily updates to keep up with the news related to Parkinson’s disease. Take advantage of lectures, seminars, conferences, and meetings that are available to you, both in your area and online.



You have a choice whether you want to look at your life from a positive perspective or one of negativity. Negativity is the best option if you want to repel friends, alienate those who are close to you, and pull yourself down. Parkinson’s has taught me not to take life for granted and to appreciate the “small things”, that really aren’t small, at all! Whether it’s a good meal, the sun on your face, or a favorite song on the radio, we must remember to celebrate the good in our lives!

We have a choice in how we see the world. If we choose to focus on the negative and fail to appreciate what is right in front of us, it is very easy to miss all the good around us. I have found that this illness can be a powerful teacher about what is important in our life. Let it teach you. Learn from it and be at peace.


Stay open, keep flexible!

A tree in the wind is sure to snap if it isn’t capable of bending and swaying with the breeze. This is a fine example of how you might look at new exercises and therapies to incorporate into your life. Trying different options offers possibilities and hope.


Work with your doctors and keep informed!

Knowing your condition and having a firm understanding of your medicines empowers you for better self-care. When you and your doctors are both well-informed, you both can communicate better. Knowledge really is power! Don’t be afraid to educate yourself on your illness.


Lower your stress and everything seems to improve!

Stressanxiety, and worry are all emotions that are detrimental to people with Parkinson’s disease. Finding exercises and therapies to lower your stress level can have a very calming effect on the whole body.




Humor, fun, and small victories are vital for you and those close to you!

Remember to incorporate fun, pleasure, and enjoyment into your daily life in any way that you can. Learn to decompress, de-stress, and even relax. Make the most of the days that you feel your best!


Balance, moderation, gratitude, compassion, and patience play a big part in staying well!

Wellness is about balancing the mind, body, and spirit and keeping the three healthy. Yoga, Reiki, meditation, and massage can be very helpful in finding the balance in your life, that you seek.


Rather than asking “why me?” ask “what can I do today for myself and others?”

Helping others helps ourselves! If we feel sorry for ourselves, we fail to see the many lessons that illness unveils. Don’t forget to be grateful for the good in your life! Rather than asking questions that really have no answer, ask yourself how you can help yourself and others in a similar situation.


Boost Your Brain Health

Parkinson's disease (PD) is a "movement" disorder because its most recognizable symptoms are tremor, slowness, stiffness and, for some, walking and balance problems. But it's also very much a "non-movement" disorder. Some of the most common and bothersome symptoms are mood and sleep changes, fatigue, and thinking and memory (cognitive) problems. Not everyone experiences cognitive changes. And, like all PD symptoms, when and how they occur is unique to each person. Some people have mild changes that don't interfere with everyday life, while others have significant problems that affect their ability to shower, put on clothes or prepare meals.

Many people, Parkinson's or not, worry about potential cognitive change as they get older. But you can take steps to keep your brain as healthy as possible. Researchers have not yet proven ways to prevent or slow cognitive change,

Be Socially Active

Spending time with friends and loved ones and meeting new people not only prevents isolation that can come with Parkinson's, but also gives you a chance to work out your brain. At social gatherings, for example, you can remember new names and discuss current events. Getting involved in PD circles is another way to connect. Find an activity that fits in your schedule, interest and comfort level -- join a support group, advocate for Parkinson's policy or participate in research.

Train Your Brain

Your brain is a bit like your muscles -- it needs a regular workout to stay in shape. Play "brain games" online; do crossword or jigsaw puzzles (get a group together so you can socialize too!); learn to speak a second language or play a new instrument; or take up a new hobby.

Reduce Stress

Everyone experiences stress in different ways and to different degrees. Common stressors are work, family and balancing the two. Stress can worsen Parkinson's symptoms and cause temporary thinking and memory changes. Identify your stressors and find ways to relieve them. Meditate, practice mindfulness, go for daily walks, or spend time gardening or relaxing in nature.

Sleep Well

Researchers believe we store memories and rejuvenate our bodies during sleep. Not getting enough rest can make it harder to manage Parkinson's and to think clearly. (Most of us have experienced the fogginess and slowness that can follow a poor night's sleep.) Make sure you sleep the recommended number of hours each night for someone your age. If you have trouble sleeping (common in PD), ask your doctor about ways to improve your rest.

Care for Medical Conditions

Diabetes, high blood pressure and high cholesterol can damage brain blood vessels and lead to thinking and memory problems. Depression and anxiety, common Parkinson's non-movement symptoms,

can cause or worsen cognitive problems. If you have one of these conditions, or you or a loved one notice mood changes, talk to your doctor. Treatment strategies may include diet adjustment, exercise, medication and, for depression and anxiety, talk therapy.

Review Your Medications

Certain prescription and over-the-counter medications, such as the Parkinson's drug Artane (trihexyphenidyl), pain or sleep pills, and even Benadryl, can cause confusion. At every, or every other visit, go through your medication list with your doctor. If any drug could cause cognitive difficulties ask whether you can stop it or decrease the dose. Always speak with your doctor before making changes or adding over-the-counter medications or supplements.

Stay tuned for more information and tips on Parkinson's and cognition later this year.

The medical information contained in this newsletter is for general information purposes only. The Michael J. Fox Foundation for Parkinson's Research has a policy of refraining from advocating, endorsing or promoting any drug therapy, course of treatment, or specific company or institution. It is crucial that care and treatment decisions related to Parkinson's disease and any other medical condition be made in consultation with a physician or other qualified medical professional.



REM Sleep Behavior Disorder Predicts Parkinson's Disease

Research has linked a particular sleep disorder called rapid eye movement (REM) sleep behavior disorder with a diagnosis of Parkinson's disease. What characterizes this sleep problem, and can its presence be a good way to predict Parkinson's risk?

Data from the National Institutes of Health (NIH) indicate that every year, approximately 50,000 people in the United States learn that they have Parkinson's disease, a neurological condition that affects a person's motor function and exposes them to other neurodegenerative problems, such as Alzheimer's disease.

Researchers still do not fully understand exactly what causes Parkinson's disease, but they have identified a few risk factors that can predispose a person to develop this condition.

These include a person's age and sex as well as some genetic factors. Still, it remains a challenge to establish early on who is likely to develop Parkinson's disease at some point in their life.

However, a team of researchers from McGill University in Montreal, Canada decided to see if one particular factor — a sleep disorder called REM sleep behavior disorder (RBD) — could be a good predictor of risk.

This sleep problem is called RBD because it occurs during the REM phase of sleep, in which a person's body becomes effectively paralyzed. This inability to move prevents the person from physically acting out any dream that they may be experiencing and thus stops them from potentially harming themselves or others.

People with RBD do not have this paralysis, which means that they end up acting out their dreams without any notion that they are doing so.

Research has shown that many people with RBD go on to develop Parkinson's disease, so the McGill University team decided to find out whether an RBD diagnosis could accurately predict Parkinson's risk.

As lead author Dr. Ron Postuma and colleagues explain, establishing that this sleep disorder is a good predictor of Parkinson's could, in the future, allow specialists to identify at-risk people and offer them experimental therapies that could delay or prevent the onset of this neurological condition.

Sleep disorder predicts risk

To establish the strength of the connection between the two conditions, the researchers — whose recent findings appear in Brain: A Journal of Neurology — worked with 1,280 people with REM sleep behavior disorder across 24 centers of the International RBD Study Group.

The researchers assessed the participants' motor function, cognitive abilities, and sensory abilities for a number of years. After a 12-year follow-up period, they found that 73.5 percent of the people involved in this study had developed Parkinson's disease.

Moreover, participants who had started experiencing motor function issues in this period had a threefold increase in the risk of developing Parkinson's disease or related conditions, such as dementia with Lewy bodies. Also at high risk were participants who had developed cognitive impairment or started experiencing problems with their sense of smell.

These findings confirm that the presence of RBD is, indeed, a strong predictor of Parkinson's disease. All the more so, since the researchers conducted the study in centers across North America, Europe, and Asia, which means that the results apply to diverse populations.

A cheaper, quicker form of assessment

Unlike the usual method of assessing the risk of Parkinson's disease, which is called dopamine transporter imaging, the current assessment is inexpensive and easy to apply.

Dopamine transporter imaging, explain Dr. Postuma and colleagues, assesses the integrity of the dopaminergic system, which typically becomes compromised in parkinsonism and Parkinson's disease. However, this test is complex and costly. In contrast, assessing for the risk factors that the current study considers is both quick and cost efficient.

"We confirmed a very high risk of [Parkinson's disease] in people with REM sleep disorder and found several strong predictors of this progression," notes Dr. Postuma.

"As new disease-modifying treatments are being developed for [Parkinson's disease] and related diseases, these patients are ideal candidates for neuroprotective trials."

Dr. Ron Postuma




Photo Source:




Pacemaker in the brain could help patients with epilepsy and Parkinsons

Engineers and researchers at the University of California, Berkeley have developed a neurostimulator that can act as a pacemaker within the human brain. This device could detect the electrical currents within the brain and also deliver brain stimulation into the brain. This form of neurological stimulation could help patients with epilepsy and Parkinsonism, the team explains.

The results of the experiments trying the new device were published in a study that appeared in the latest issue of the journal Nature Biomedical Engineering.

The team has named the device WAND that stands for, “wireless artifact-free neuromodulation device,” and have called it the pacemaker for the brain. The researchers explain that in diseases such as epilepsy, there is an abnormal electrical activity within the brain that causes a firing across the brain which leads to whole brain involvement and seizures. Patients with tremors and other movement disorders too have abnormal brain electrical activity. Before these seizures or movement disorders are seen, there are minor triggers and these electrical signatures are often difficult to detect. The frequency of electrical stimulations that are needed to prevent these minor triggers are known to be equally tricky and low voltage. Multiple adjustments are necessary to provide optimal treatment to patients so that they benefit from the.

WAND is a device that is wireless as well as autonomous. This means that the device can pick up the subtle signs of an impending tremor or seizure from the minor electrical activities of the brain. Thereafter the device can regulate the amount of stimulation it would provide to counteract the electrical signals of the brain. This can prevent the unwanted movements as well as the seizures. The detection as well as the stimulation is all recorded by the device and thus can be adjusted with each signal.

The team used experimental rhesus macaques and used WAND to delay specific arm movements in the animals. Researchers at Cortera Neurotechnologies, Inc., have developed the integrated circuits of the WAND that could record the brain signals from both sides of the brain and also the electrical pulses. The chip on the device can separate the electrical pulses within the brain and the normal brain waves. Muller explained, “Because we can actually stimulate and record in the same brain region, we know exactly what is happening when we are providing a therapy.” The team worked in collaboration with the lab of electrical engineering and computer science professor Jan Rabaey. Rikky Muller Assistant Professor of electrical engineering and computer sciences at Berkeley explained, “The process of finding the right therapy for a patient is extremely costly and can take years. Significant reduction in both cost and duration can potentially lead to greatly improved outcomes and accessibility. We want to enable the device to figure out what is the best way to stimulate for a given patient to give the best outcomes. And you can only do that by listening and recording the neural signatures.” The device can record electrical activity over 128 channels or points across the brain. Other systems that have been developed previously could record from only eight channels. The deep brain stimulators at present can provide electrical stimulations but stop recording when they do so. This means that vital signals may be missed. WAND on the other hand keeps recording even while providing the stimulation.

Muller speaking of their experiment with the macaques said, “While delaying reaction time is something that has been demonstrated before, this is, to our knowledge, the first time that it has been demonstrated in a closed-loop system based on a neurological recording only... In the future we aim to incorporate learning into our closed-loop platform to build intelligent devices that can figure out how to best treat you, and remove the doctor from having to constantly intervene in this process.”


By Ananya Mandal, MDJan 1 2019

 Image Credit: Rikky Muller, UC Berkeley

Caffeine plus another compound in coffee beans' waxy coating may protect against brain degeneration

Rutgers scientists have found a compound in coffee that may team up with caffeine to fight Parkinson's disease and Lewy body dementia - two progressive and currently incurable diseases associated with brain degeneration.

The discovery, recently published in the Proceedings of the National Academy of Sciences, suggests these two compounds combined may become a therapeutic option to slow brain degeneration.

Lead author M. Maral Mouradian, director of the Rutgers Robert Wood Johnson Medical School Institute for Neurological Therapeutics and William Dow Lovett Professor of Neurology, said prior research has shown that drinking coffee may reduce the risk of developing Parkinson's disease. While caffeine has traditionally been credited as coffee's special protective agent, coffee beans contain more than a thousand other compounds that are less well known.

The Rutgers study focused on a fatty acid derivative of the neurotransmitter serotonin, called EHT (Eicosanoyl-5-hydroxytryptamide), found in the bean's waxy coating. The researchers found that EHT protects the brains of mice against abnormal protein accumulation associated with Parkinson's disease and Lewy body dementia.

In the current research, Mouradian's team asked whether EHT and caffeine could work together for even greater brain protection. They gave mice small doses of caffeine or EHT separately as well as together. Each compound alone was not effective, but when given together they boosted the activity of a catalyst that helps prevent the accumulation of harmful proteins in the brain. This suggests the combination of EHT and caffeine may be able to slow or stop the progression of these diseases. Current treatments address only the symptoms of Parkinson's disease but do not protect against brain degeneration.

Mouradian said further research is needed to determine the proper amounts and ratio of EHT and caffeine required for the protective effect in people.

"EHT is a compound found in various types of coffee but the amount varies. It is important that the appropriate amount and ratio be determined so people don't over-caffeinate themselves, as that can have negative health consequences," she said.

More to come....


 Picture source:

MarkSweep - released into public domain Uploaded: 13 January 2005

Parkinson's Disease Compared to Dementia with Lewy Bodies (DLB)

Parkinson’s disease is a motor illness that progresses gradually. It affects the dopamine-producing neurons responsible for body movements. Dementia with Lewy bodies (DLB), on the other hand, is a disease that leads to a progressive decline in mental abilities. Some may mistake the symptoms of DLB with Parkinson’s because of the common symptoms of muscle rigidity and slow movements.

Parkinson’s Disease in a Nutshell

Parkinson’s disease is a neurodegenerative disease affecting about 1 to 2 percent of people over the age of 60 years. Worldwide, an estimated 10 million people have been diagnosed with Parkinson’s disease. In the United States, 60,000 people are being diagnosed every year and at present, about one million people are living with the condition.

In Parkinson’s disease, the dopamine-producing nerves of the brain gradually die. When dopamine levels decrease, the symptoms of Parkinson’s disease develop, and movement is impaired.

Though the exact cause of PD is unclear, some risk factors have been identified. For instance, genetics play a role, as do certain environmental triggers such as the exposure to toxins.

Dementia with Lewy Bodies (DLB) Overview

In some cases, however, brain changes may lead to the development of movement symptoms. Lewy bodies are clumps of abnormal deposits in the brain of a protein called alpha-synuclein. Accumulation of these deposits leads to problems with movement, thinking, mood, and behavior.

Dementia with Lewy bodies (DLB) is a progressive type of dementia that involves the formation of Lewy bodies in the nerve cells. DLB is the third most common cause of dementia, after Alzheimer’s disease and vascular dementia. About 10 to 25 percent of all cases of dementia are due to DLB.

In DLB, patients may have signs and symptoms of impaired thinking, memory loss, inability to understand visual information, changes in reasoning, or fluctuations in cognition and attention. Also, patients may have difficulty with movement (including walking), tremors, slowness, and muscle stiffness. Some patients may have trouble sleeping, visual hallucinations, delusions, and balance problems.About 1.3 million Americans are living with DLB. However, there is limited information about incidence, as it is thought to be severely underdiagnosed. Some cases are misdiagnosed as other types of dementia or even Parkinson’s disease.

Difference Between Parkinson’s Disease and Dementia with Lewy Bodies (DLB)

Parkinson’s disease involves problems with movement. Although DLB is characterized by movement issues, it is often accompanied by other symptoms.


Parkinson’s disease and DLB may both involve show evidence of Lewy bodies in neurons in the brain. Lewy bodies are groups of proteins called alpha-synuclein, a naturally occurring protein in the brain, that is associated with various brain changes at high levels.

The exact reason for the large protein buildup is unknown. However, the more clumps of Lewy bodies develop, the increased the risk of nerve cell damage and death. Lewy bodies are also seen in Parkinson’s disease.


Though both disorders may involve the presence of Lewy bodies, some patients with Parkinson’s disease may only experience a mild cognitive decline. Most patients with PD only experience problems with mobility. However, there are cases in which patients with PD develop cognitive decline and dementia as a complication of the disease.

When dementia occurs after a diagnosis of a motor disorder, it’s dubbed as Parkinson’s disease with dementia (PDD). In contrast, if the cognitive decline and memory loss occur before or at the same time as the development of a motor disorder, it’s called DLB.

PDD and DLB are sometimes referred to collectively as Lewy body dementias. There is no cure for either disease, but treatments aim to slow disease progression.

3D illustration showing neurons containing Lewy bodies small red spheres which are deposits of proteins accumulated in brain cells that cause their progressive degeneration. 

Image Credit: Kateryna Kon / Shutterstock

By Angela Betsaida B. Laguipo, BSNReviewed by Jennifer Logan, MD, MPH  

The appendix may be associated with Parkinson’s disease

The vermiform appendix or appendix as we commonly know it, is a vestigial organ of the body which does not come into notice unless it is inflamed (such as in appendicitis). In cases of appendicitis, the finger like part of the gut at the base of the caecum is surgically removed.

Now researchers have come up with a finding that this appendix may play a role in Parkinson’s disease.

The study, 'The vermiform appendix impacts the risk of developing Parkinson’s disease', is published in the latest issue of the journal Science Translational Medicine.

The researchers from United States have found that the appendix may contain a substance that might be killing brain cells to cause Parkinson’s disease. In this condition there are toxic proteins that are built up in the brain. These areas of the brain are linked to normal movements which are affected. Parkinson’s disease affects thousands worldwide and is incurable and progressive. According to charity Parkinson’s UK, this study is a revelation because it shows that the origin of the disease condition may lie outside the brain.

For this study the team of researchers from the Van Andel Research Institute, in Michigan looked at health data from 1.7 million individuals over around 50 years. They noted that people who had had their appendix removed surgically were at a 20 percent lower risk of getting Parkinson’s disease. The team analysed 847 people with Parkinson’s disease as well. Among these 54 had their appendixes removed. Results revealed that those who had had their appendices removed showed the symptoms of Parkinson’s disease an average of three and half years later than those who had their appendices.

The team looked at the contents of the appendix and found that it contained a toxic protein called alpha synuclein. Incidentally the brains of Parkinson’s disease patients also contain high amounts of this toxic protein. The chemical structure of the protein found in the appendix of a Parkinson’s patient was found to be different from what was found in healthy persons, the researchers noted. Although experts as well as researchers have warned that the appendix may not be the only organ to blame, they have said that the gut needs to be looked at carefully. The gut may contain toxic proteins that travel up to the brain via the vagus nerve to cause neurodegenerative conditions.

Dr Viviane Labrie, an assistant professor at Van Andel Research Institute in Michigan and senior author of the study, said that this study does not recommend all people to undergo an appendectomy (surgical removal of appendix) to protect themselves from Parkinson’s disease. She said, “It would be much more wise to control or dampen excessive formation of alpha synuclein to tune down the overabundance or potentially to prevent its escape.” She explained that drug therapies could target this finding to prevent Parkinson’s disease. She added that the appendix actually may play a role in the body’s immune system as well.

Claire Bale, from Parkinson’s UK in a statement said, “This research is really important because it gives us some of the most compelling evidence yet that Parkinson's may begin outside the brain, which is a revolutionary new idea that is emerging in the scientific world. Understanding where and how Parkinson's begins will be absolutely crucial to developing treatments that can stop it and potential prevent it altogether.”

The study was supported by Michael J Fox Foundation for Parkinson's Research and Shake it Up Australia Foundation.

Appendix Illustration. 3D rendering. Image Credit: Nerthuz / Shutterstock



Acknowledge, assess and treat early!

The time between diagnosis and the institution of symptomatic treatment is critical in the effort to find a cure for Parkinson's Disease (PD). A paper published in npj Parkinson's Disease notes too many early PD patients wait too long before seeking medical attention, or start taking symptomatic medications before they are required, thereby dramatically shrinking the pool of candidates for clinical trials. The pace of progression varies among patients, making the months following diagnosis crucial to researchers studying the disease's progression.

"The critical time of about one year from when the patient can be diagnosed with early PD based on mild classic motor features until they truly require symptomatic therapy can be considered the Golden Year," said lead author Robert A. Hauser, MD, director of the Parkinson's & Movement Disorder Center at the University of South Florida. "It is during this early, untreated phase, that progression of clinical symptoms reflects the progression of the underlying disease."

Hauser says that in order to determine whether or not a potential disease slowing therapy is actually working, they must be able to compare the therapy to a placebo without interference from symptomatic treatment. Otherwise, they won't know if the therapy is slowing the disease's progression or if they are just seeing the effects of symptomatic treatment.

This requires patients to seek assessment soon after they notice the onset of tremor or slow movement. In addition, physicians should consider referring patients to clinical trials soon after diagnosis and delay prescribing symptomatic medication until it's necessary. If a patient waits until symptomatic treatment is necessary, the opportunity to participate in these crucial clinical trials is lost.




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Promise in stem cell research for Parkinson’s disease

Cell-replacement or stem cell therapy shows some promise as a treatment for Parkinson's. A recent paper in the journal Molecular & Cellular Proteomics reports a technical advance in selecting cells to use in this therapy.

Cell-replacement (stem cell) therapy involves differentiating stem cells into dopamine-signaling, or dopaminergic, neurons and transplanting them into a patient's brain to replace dying neurons. However, the variability of how the cells evolve (what specialty functions the cells learn) can affect transplantation outcomes. In clinical trials in the 1990s, for example, such contamination gave some patients severe dyskinesia, uncontrollable jerky movements that were worse than the movement problems caused by Parkinson's disease.

To avoid interference by unwanted cell types, researchers needed a differentiation protocol that yielded a more homogeneous (neutral/cleaner) population of dopaminergic neurons. Researchers led by Hossein Baharvand, of Iran's University of Science and Culture in Tehran, and Ghasem Hosseini Salekdeh, of the Academic Center for Education, Culture and Research in Iran and Macquarie University in Australia, set out to develop such a protocol.

First, the team developed a special stem cell line that contained a green fluorescent protein, or GFP, reporter for a transcription factor involved in dopaminergic neuronal development. In undifferentiated cells from this line, the fluorescent reporter is not expressed. When cells begin to make the transcription factor, the first step toward becoming a dopaminergic neuron, they begin to make the GFP protein. So essentially the scientists could take the undifferentiated cells and tell which ones would become good dopamine signaling cells over time by color of protein excreted as they changed. They then isolated those cells and transplanted them into rats modeling Parkinson's disease. Rats that received transplants with those cells had better dopamine release, indicating that the transplanted cells were a better match for the dying neurons they were meant to replace. Sorting the cells also reduced motor symptoms of Parkinson's compared with rats treated that received unsorted cells.

This is a major breakthrough in the idea of stem cell use for the treatment of Parkinson’s disease and shows promise for possible future use.




Parkinson's disease - - immune mediated disease?

Scientists are working to gain insights into the mechanisms which lead to the loss of nerve cells that produce dopamine. Until now, little has been known about whether human immune cells have an important role to play in Parkinson's disease. The stem cell researchers Dr. Annika Sommer, Dr. Iryna Prots and Prof. Dr. Beate Winner from FAU and their team have made a major leap forward in research into this aspect of the disease. The scientists from Erlangen were able to prove that in Parkinson's disease immune cells from the immune system, so-called t-cells, attack and kill nerve cells which produce dopamine in the midbrain.

The FAU team based its research on a surprising observation: the scientists found an unusually high number of t-cells in the midbrain of Parkinson's patients. These cells are commonly found in the brains of patients suffering from diseases in which the immune system attacks the brain. During tests carried out in collaboration with the movement disorders clinic (molecular neurology) at Universitätsklinikum Erlangen (Prof. Jürgen Winkler), researchers discovered an increased number of certain t-cells, specifically Th17 cells, in Parkinson's patients, similar to patients with autoimmune diseases such as rheumatoid arthritis.

In view of these results, the researchers decided to develop a very unusual cell culture from human cells. A small skin sample was taken from affected patients and healthy test subjects. These skin cells were converted into stem cells, which can develop into any type of cell. The research team then further differentiated these cells into midbrain nerve cells specific to the patient. These midbrain nerve cells were then brought into contact with fresh t-cells from the same patients. The result: the immune cells of Parkinson's patients killed a large number of their nerve cells, but this did not appear to be the case with healthy test subjects. Another result gives reason for hope: antibodies which block the effect of Th17 cells, including one antibody which is already being used on a daily basis in the hospital to treat psoriasis, were able to largely prevent the death of the nerve cells.

'Thanks to our investigations, we were able to clearly prove not only that t-cells are involved in causing Parkinson's disease, but also what role they actually play,' explains Prof. Dr. Beate Winner. 'The findings from our study offer a significant basis for new methods of treating Parkinson's disease.'


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Vitamin B3 the next treatment for Parkinson’s?

Researchers from the Hertie Institute for Clinical Brain Research have shown that a form of vitamin B3 called nicotinamide riboside may offer a possible treatment for Parkinson’s disease. Dr Michela Deleidi who led the research says the substance stimulates the faulty energy metabolism in affected nerve cells and protects them from dying off.

Although the precise cause of Parkinson’s is not fully understood, scientists know that nerve cells in the substantia nigra region of the brain die off die to damaged mitochondria (the energy producing organelles in a cell). Goal of the study was to investigate whether damaged mitochondria were merely a side effect or whether they cause Parkinson's disease

Working with international colleagues, Deleidi and team took skin cell samples from patients with Parkinson’s disease and induced them to turn into stem cells, which then developed into nerve cells. The cells had a defect in the GBA gene, the most common risk gene for Parkinson’s. These defected nerve cells had damaged mitochondria and, consequently, impaired energy production. The researchers then tried to stimulate the formation of new mitochondria, a process that involves a coenzyme called NAD. They added a form of vitamin B3 called nicotinamide riboside, a preliminary stage of the coenzyme, to the cells. As described in Cell Reports, an increase in the cellular level of NAD resulted in the formation of new mitochondria and an increase in energy production. Next, the team investigated the effects of feeding the vitamin to flies with a GBA gene defect. The death of nerve cells in these flies causes them to have increasing difficulty walking and climbing as they aged.


Deleidi and colleagues divided the flies into two groups: those that received feed enriched with nicotinamide riboside and those that did not. The substance seemed to have a positive effect, with far fewer nerve cells dying off.  The flies also retained their mobility for longer. Deleidi says the results suggest that the loss of mitochondria does indeed play a significant role in the genesis of Parkinson’s disease and that administering nicotinamide riboside may be a new starting-point for treatment. Further studies are needed to establish whether the vitamin can really treat Parkinson’s and the researchers are planning to test the effects of nicotinamide riboside on patients.



Image Credit: Kateryna Kon / Shutterstock

August Shared Road.jpg

Study links pesticide exposure to increased risk of developing Parkinson's disease

A new University of Guelph study has discovered why exposure to pesticides increases some people's risk of developing Parkinson's disease.

Previous studies have found an association between two commonly used agrochemicals (paraquat and maneb) and Parkinson's disease.

Now U of G professor Scott Ryan has determined that low-level exposure to the pesticides disrupts cells in a way that mimics the effects of mutations known to cause Parkinson's disease.

Adding the effects of the chemicals to a predisposition for Parkinson's disease drastically increases the risk of disease onset, said Ryan.

"People exposed to these chemicals are at about a 250-percent higher risk of developing Parkinson's disease than the rest of the population," said Ryan, a professor in the Department of Molecular and Cellular Biology.

"We wanted to investigate what is happening in this susceptible population that results in some people developing the disease."

Used on a variety of Canadian crops, paraquat is used on crops as they grow and maneb prevents post-harvest spoiling.

Published in the journal Federation of American Societies for Experimental Biology, this study used stem cells from people with Parkinson's disease that had a mutation in a gene called synuclein that is highly associated with increased risk of Parkinson's Disease, as well as normal embryonic stem cells in which, the risk associated mutation was introduced by gene editing.

"Until now, the link between pesticides and Parkinson's disease was based primarily on animal studies as well as epidemiological research that demonstrated an increased risk among farmers and others exposed to agricultural chemicals," said Ryan. "We are one of the first to investigate what is happening inside human cells."

From the two types of stem cells, Ryan and his team made dopamine-producing neurons -- the specific neurons affected in Parkinson's disease -- and exposed them to the two agrochemicals.

In exposing cells to agrochemicals, energy-producing mitochondria were prevented from moving to where they were needed inside the cell, depleting the neurons of energy.

Neurons from the Parkinson's patients and those in which the genetic risk factor was introduced were impaired at doses below the EPA reported lowest observed effect level. Higher doses are needed to impair function in normal neurons.

"People with a predisposition for Parkinson's disease are more affected by these low level exposures to agrochemicals and therefore more likely to develop the disease," said Ryan. "This is one of the reasons why some people living near agricultural areas are at a higher risk."

He said the findings indicate that we need to reassess current acceptable levels for these two agrochemicals.

"This study shows that everyone is not equal, and these safety standards need to be updated in order to protect those who are more susceptible and may not even know it."



Study: People taking immunosuppressant drugs less likely to develop Parkinson's disease

People who take drugs that suppress the immune system are less likely to develop Parkinson's disease, according to a study from Washington University School of Medicine in St. Louis.

The findings, published May 31 in Annals of Clinical and Translational Neurology, suggest that a person's own immune system helps nudge him or her down the path toward Parkinson's. Restraining the immune system with drugs potentially could prevent the neurological disorder, which is characterized by tremors, slow movements, stiffness and difficulty walking.

Last year, medical researchers analyzed millions of medical records and developed an algorithm to predict which people would be diagnosed with the disease. As they mined the data, they discovered that people with several types of autoimmune diseases, including ulcerative colitis, were less likely to be diagnosed with Parkinson's than the general population. The autoimmune diseases were a mixed bag, linked to myriad glitches in the immune system and affecting a variety of organ systems. It was hard to see how such a hodgepodge of immune system malfunctions all could end up having the same beneficial effect.

The researchers noted, however, that many autoimmune diseases do have one thing in common: They are treated with drugs that dampen immune activity. Having an autoimmune disease may not be a good thing, but being treated for one might be, they decided.

Researchers then analyzed Medicare Part D prescription drug data on 48,295 people diagnosed with Parkinson's in 2009 and 52,324 people never diagnosed with Parkinson's. They identified 26 commonly prescribed immunosuppressant drugs, representing six classes of medications. The researchers determined which people in the data set had been prescribed any of the drugs a year or more before the date of diagnosis or by a pre-set cutoff date. Prescriptions written in the 12 months before diagnosis or by the cutoff were excluded to rule out any chance that the prescriptions might have been linked to early signs of the disease.

The researchers found that people taking drugs in either of two classes were significantly less likely to develop Parkinson's than those taking no immunosuppressants. People taking corticosteroids such as prednisone were 20 percent less likely to be diagnosed with Parkinson's, while those on inosine monophosphate dehydrogenase (IMDH) inhibitors were about one-third less likely.

When the researchers included specific autoimmune diseases in their analysis, the calculated risks didn't change, suggesting that the difference was due to use of the drugs, not the underlying diseases they were treating.

The findings suggest that tamping down immunity with drugs may keep Parkinson's disease at bay. But doing so also makes people more susceptible to infectious diseases and cancer. The benefits of immunosuppressive drugs outweigh the costs for people with serious autoimmune diseases like rheumatoid arthritis. But doctors probably would hesitate to prescribe risky drugs to healthy people to stave off Parkinson's, especially since there is no reliable way to predict who is on track to develop the disease. The newest theory is that if a drug reduces the risk of getting Parkinson's, it also will slow disease progression, and researchers are exploring that now.


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10th Annual Community Parkinson's Symposium

The 10th annual community Parkinson's Symposium was a SMASHING success!! Thank you to all that attended this amazing event. I know that it was long but there was so much wonderful information shared and resources available, it was hard to limit the time! We had 283 attendees, 54 vendors and 23 volunteers!!! Between the Silent auction and table top donations, we were able to raise almost $3,000!!! Thanks to all of you, this is one that will be known as one of the best.

Please browse through all of the awesome pictures posted on this site, as well as the presentations from the fantastic speakers. If you did not give contact information and wish to be on our mailing or emailing lists, please let us know!

Thank you again!

Midwest Parkinson's Initiative

Research suggests that Vitamin B12 supplementation could postpone disease progression in Parkinson’s patients

Patients recently diagnosed with Parkinson’s disease that have low levels of vitamin B12 develop symptoms faster than those with higher levels, suggesting supplementation could postpone the progression of symptoms, new research has found.

The study, published in the journal Movement Disorders, demonstrates that low vitamin B12 levels are associated with greater walking and balance problems, possibly due to the known effect of a B12 deficiency on the central peripheral nervous systems.

Researchers divided patients, who were recently diagnosed but had not yet begun treatment, into three groups according to their levels of vitamin B12 and assessed them over a two-year period.

Upon completion of preliminary evaluations, patients were given the opportunity to take a controlled daily vitamin supplement.  Research results showed improved vitamin B12 levels in approximately 50% of participants, indicating supplementation was taken.

Disease progression in patients with improved vitamin B12 levels was found to be much slower with them exhibiting a decreased score on the Unified Parkinson’s Disease Rating Scale (UPDRS) (a measure of Parkinson’s disability) compared with those maintaining low levels of the vitamin.

A deficiency of this essential vitamin promotes the development of neurological and motor symptoms associated with Parkinson’s disease, including depression, paranoia, muscular numbness and weakness.

Known as the brain booster, vitamin B12 is vital for cognitive health, however it is notoriously difficult to absorb through the gut, meaning that supplementing has become a necessity.  In fact, B12 is so difficult to absorb that only one percent of intake from food is retained.

Supplementing B12 via a daily oral spray means the vitamin is absorbed directly into the bloodstream, avoiding the digestive system which can destroy essential nutrients with strong enzymes and acids.

Andrew Thomas, founder and managing director of natural health company BetterYou, said:

B12 is a vital nutrient, by delivering it orally in spray form it benefits from the superabsorbent soft tissue of the mucosal membrane within the mouth and the proximity of a rich vascular system.

Our daily required intake for health maintenance is relatively small, however few foods provide a rich source (red meats and offal are major sources) and more restricted diets omit these. In addition, B12 is a very difficult vitamin to absorb and our digestive efficiency is reducing rapidly.

Supplementation is becoming more of a necessity for us and using a spray in the mouth bypasses the digestive system, ensuring optimal absorption.

BetterYou B12 Boost Oral Spray uses the most bio available form of B12 (Methylcobalamin), which is a naturally active form found within human metabolism meaning it is processed faster by the body than most other forms found in supplements.

More research is needed to determine degree this may affect Parkinson's symptom progression. 


Calcium levels in the blood linked to the development in Parkinson's

Researchers have found that excess levels of calcium in brain cells may lead to the formation of toxic clusters that are the hallmark of Parkinson's disease.

The international team, led by the University of Cambridge, found that calcium can mediate the interaction between small membranous structures inside nerve endings, which are important for neuronal signalling in the brain, and alpha-synuclein, the protein associated with Parkinson's disease. Excess levels of either calcium or alpha-synuclein may be what starts the chain reaction that leads to the death of brain cells.

The findings, reported in the journal Nature Communications, represent another step towards understanding how and why people develop Parkinson's. Parkinson's disease is one of a number of neurodegenerative diseases caused when naturally occurring proteins fold into the wrong shape and stick together with other proteins, eventually forming thin filament-like structures called amyloid fibrils. These amyloid deposits of aggregated alpha-synuclein, also known as Lewy bodies, are the sign of Parkinson's disease.

Curiously, it hasn't been clear until now what alpha-synuclein actually does in the cell: why it's there and what it's meant to do. It is implicated in various processes, such as the smooth flow of chemical signals in the brain and the movement of molecules in and out of nerve endings, but exactly how it behaves is unclear.

"Alpha-synuclein is a very small protein with very little structure, and it needs to interact with other proteins or structures in order to become functional, which has made it difficult to study," said senior author Dr Gabriele Kaminski Schierle from Cambridge's Department of Chemical Engineering and Biotechnology.

Thanks to super-resolution microscopy techniques, it is now possible to look inside cells to observe the behavior of alpha-synuclein. To do so, Kaminski Schierle and her colleagues isolated synaptic vesicles, part of the nerve cells that store the neurotransmitters which send signals from one nerve cell to another.

In neurons, calcium plays a role in the release of neurotransmitters. The researchers observed that when calcium levels in the nerve cell increase, such as upon neuronal signalling, the alpha-synuclein binds to synaptic vesicles at multiple points causing the vesicles to come together. This may indicate that the normal role of alpha-synuclein is to help the chemical transmission of information across nerve cells.

"This is the first time we've seen that calcium influences the way alpha-synuclein interacts with synaptic vesicles," said Dr Janin Lautenschluger, the paper's first author. "We think that alpha-synuclein is almost like a calcium sensor. In the presence of calcium, it changes its structure and how it interacts with its environment, which is likely very important for its normal function."

"There is a fine balance of calcium and alpha-synuclein in the cell, and when there is too much of one or the other, the balance is tipped and aggregation begins, leading to Parkinson's disease," said co-first author Dr Amberley Stephens.

The imbalance can be caused by a genetic doubling of the amount of alpha-synuclein (gene duplication), by an age-related slowing of the breakdown of excess protein, by an increased level of calcium in neurons that are sensitive to Parkinson's, or an associated lack of calcium buffering capacity in these neurons.

Understanding the role of alpha-synuclein in physiological or pathological processes may aid in the development of new treatments for Parkinson's disease. One possibility is that drug candidates developed to block calcium, for use in heart disease for instance, might also have potential against Parkinson's disease.


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The gut-brain axis....what does that mean?

There is growing recognition within the medical and scientific communities of the link between the microbial composition of the intestines and the central nervous system, known as the “gut-brain axis”. This encompasses bidirectional communication channels between the central nervous system, the enteric nervous system, and the endocrine system.

Moreover, the gut-brain axis is responsible for the regulation of immune responses in both the intestines and the brain, with all aspects being heavily affected by the activity of intestinal microorganisms. It is no wonder then that dysregulation of gut microbiota may lead to various disturbances and diseases in the human body.

However, there are still a lot of question marks regarding both the content and repercussions of this dialogue between the central nervous system and the gastrointestinal system. Intestinal health can influence the brain, and research is pointing towards chronic intestinal inflammation as a potential culprit in neurodegenerative conditions such as Alzheimer's and Parkinson’s disease

In Parkinson’s disease, intestinal dysregulation is usually observed several years prior to the clinical manifestation of the illness. Some novel hypotheses state that the condition originates in the gut and then spreads to the brain through the gut-brain axis – more specifically, via stimulation of the vagus nerve and the spinal cord. This is supported by the fact that the parasympathetic vagal fibers that  innervate the intestine (among other regions) emerge from the dorsal motor nucleus.

Researchers are interested in understanding the influence of the gut microbiota in regard to Parkinson’s disease. One early study where fecal microbiota samples were acquired from 72 individuals with Parkinson’s disease and their age-matched controls revealed increased numbers of Enterobacteriaceae and reduced numbers of Prevotellaceae in affected individuals.

Moreover, excessive manganese is a putative risk factor in cases of environmentally-linked Parkinson’s disease. Metal toxicity may influence gut motility and, consequently, alter the production of key microbial metabolites in the gut. Therefore it is highly likely that exposure to toxins in the environment can influence the profile of the gut microbiome producing possible unfavorable effects on the central nervous system.



Clinically used drug, Niclosamide, could make the difference in Parkinson's disease

Researchers at Cardiff University, in collaboration with the University of Dundee, have identified a drug molecule within a medicine used to treat tapeworm infections which could lead to new treatments for patients with Parkinson's disease.

Over the last decade or so, researchers striving to find a cure for this debilitating disease have focused their attention on a protein found in the human body known as PINK1. It's understood that the malfunction of this protein is one of the leading causes of Parkinson's disease.

Several studies have suggested that discovering a drug which is capable of enhancing the function of PINK1 could be a significant step in halting neurodegeneration and therefore slow down or even treat Parkinson's disease.

With this knowledge in mind, researchers at Cardiff and Dundee Universities have discovered that a drug traditionally used to treat tapeworm infections, named Niclosamide, is also an effective activator of the PINK1 protein.

Furthermore, the research, funded by The Welcome Trust, revealed that Niclosamide and some of its derivatives could enhance PINK1 performance within cells and neurons. This has given the researchers reason to believe that this drug could provide new hope for patients living with Parkinson's disease. This is the first report of a clinically used drug that could be used to activate PINK1 and may hold promise in treating Parkinson's disease.