St. Luke’s holding “Polka for Parkinson’s” dance at Musikfest Cafe

THE MORNING CALL |APR 05, 2019

St. Luke’s University Health Network is sponsoring “Polka for Parkinson’s,” an afternoon of fun, camaraderie, education and healing for people with Parkinson’s disease and their families.

The dance, which runs from 1-4 p.m. Sunday at ArtsQuest’s Musikfest Cafe, features old world polka music and waltzes, as well as appearances by Button Box Committee and famed accordion player Walt Groller. It has been held annually in April since 2013, in observance of Parkinson’s Disease Awareness Month.

Polka-dancing can reduce symptoms and slow the progression of the neurological brain disorder, St. Luke’s said in a news release.

“Movement in general, staying active, can have a huge impact on a patient with Parkinson,” Dr. Aaron Lasker, a neurologist and medical director of St. Luke’s Movement Disorders Center, said in the release.

“It can actually slow the progression of Parkinson’s disease.”

Parkinson’s strikes mostly men, typically in their 60s and 70s, but can occur at younger ages, as was the case for actor Michael J. Fox, who has lived with the disease for nearly three decades after being diagnosed at age 29.

It occurs when nerve cells that produce dopamine are damaged or die, disrupting muscle movements, the release said. People with Parkinson’s may have limb tremors, and difficulty with walking, balance and speech. Symptoms get worse with time and there is no cure.

St. Luke’s also holds “Big and Loud” exercises classes, where patients with Parkinson’s can work out together; a monthly support group; and monthly patient education lectures.

Dance is a particularly good exercise for balance, enabling patients to practice forward and backward movement, and to work on symptoms such as freezing, which is when a person feels stuck in place.

Polka music provides cues which unblock freezing, the release said. Patients can use the beat with freezing episodes off the dance floor, too.

“I can certainly see the positive long-term effects in patients who incorporate dancing and exercise into their lives,” Dr. Nancy Diaz-Pechar, a movement disorder specialist at St. Luke’s, said in the release.

If interested in attending, St. Luke’s asks that you register at 1-866-785-8537. A $5 suggested donation will go to St. Luke’s Parkinson’s Disease Fund.

https://www.mcall.com/health/mc-hea-stluke-polka-parkinson-20190405-6cjukas5e5egpgxrazmpqpnnja-story.html

Woman helps people cut loneliness with 'Cafe Conversations'

 CBS    Apr 05, 2019

LONDON (CBS) Even in a busy place like London, filled with nearly 9 million people, loneliness can take its toll.

''Sometimes being in a big city, you're even more isolated. You're surrounded by people, but you don't know who to talk to," said Louise Kaye, the creator of Cafe Conversations.

For Kaye, loneliness hit when her husband was diagnosed with Parkinson's disease.

She talked her local restaurant into opening its doors to a social idea.

"I just kept my fingers crossed that people would turn up," she said.

And they did.

Cafe Conversations is now a weekly meetup for strangers who have learned to connect over a cup of coffee or tea. Brought together by loneliness, the group talks about anything but. Questions keep the conversation flowing.

''You don't have to say anything. You talk as much as you'd like about whatever you like," said Diane Johnson, a conversation starter.

A new poll from Michigan researchers reveals loneliness shows up most in people 50-80 who also have health issues and unhealthy eating habits. Previous studies linked chronic loneliness to problems including memory loss and shorter lives.

Sausan Sulimn struggled to find a place in the British capital after fleeing from Syria.

Reporter: After you've been to a cafe conversation, how do you feel?

Sausan Sulimn: I feel so happy.

Reporter: So less lonely?

Sausan Sulimn: Yes, absolutely.

After seeing the friendships formed through these cafe conversations, Kaye hopes the concept will catch on around the world, making people feel less alone one cup at a time.

The campaign to fight loneliness is spreading across the UK. An English bus service launched a "Chatty Bus" route, where volunteers strike up conversations with lonely passengers.

Video:

https://www.wcax.com/content/news/Woman-helps-people-cut-loneliness-with-Cafe-Conversations-508174431.html?ref=431

Veteran Raising Awareness about Unexpected Parkinson’s Symptoms

April 5, 2019

Dan McFarland is raising awareness about Parkinson's non-movement symptoms.

(StatePoint) Dan McFarland’s family was concerned when he started taking pictures of clouds and posting them on social media with urgent messages about how they were symbols about the need to repent and get ready for the end of the world. His frequent bouts of paranoia and experience with surprising visions seemed out of character, especially since McFarland was a successful businessman, running one of the largest retirement communities in Oregon, and a retired U.S. Air Force senior master sergeant.

It turned out that these delusions and hallucinations were non-motor symptoms of Parkinson’s disease, which McFarland had been diagnosed with years before. For McFarland, these symptoms were harder to manage than the motor symptoms typically associated with Parkinson’s disease, such as tremors, rigidity or slowness of movement.

“My neurologist was able to recognize my non-motor symptoms of Parkinson’s. Some of my hallucinations and delusions were frightening to me and upsetting to my loved ones, and adjusting my treatment helped lessen this burden,” he says. “To help others recognize these symptoms, I’ve gotten involved in my local Parkinson’s support group, and am sharing my story during April, which is Parkinson’s Disease Awareness Month.”

Although there is no clear understanding of the exact cause of hallucinations and delusions associated with Parkinson’s, around half of all people with Parkinson’s may experience these symptoms over the course of their disease.

For McFarland, when he first began to experience hallucinations and delusions, he recognized that what he was seeing and believing wasn’t quite real. But it was confusing to him and as his condition progressed, he began to lose insight. For example, his belief that the end of the world was coming was triggered by a brief news story about a sink hole in South America. He also began to distrust family and friends. After his wife left a camping trip early, he became suspicious that she might be trying to connect with an old boyfriend. In reality, she had simply needed a much-deserved break from work and caregiving responsibilities.

Left unaddressed, these non-movement symptoms can impact people with Parkinson’s and their care partners’ ability to make plans with family and friends and even sleep, according to a recent survey conducted by the Parkinson’s Movement Disorder Alliance. Experts say that if you believe you or a loved one is experiencing hallucinations or delusions as a result of Parkinson’s disease, the first step is talking to a movement disorder specialist. You can also go to MoretoParkinsons.com to learn more about what to expect and how to start the conversation with a physician.

While doctors may be able to address non-motor symptoms like hallucinations and delusions, it’s important to keep in mind that everyone is different and for some, other non-motor symptoms may still persist. McFarland continues to struggle with depression and anxiety, which are other common non-movement symptoms of Parkinson’s disease. McFarland sees a therapist to help manage those symptoms. Having a greater understanding of the disease and its possible symptoms has helped the McFarlands deal with them as they arise.

“Opening up about my fears and beliefs led to an improvement in my treatment plan and I’m experiencing fewer non-movement symptoms,” says McFarland. “I hope that my story will encourage others to recognize these symptoms in themselves and others, because there are options to help.”

http://www.news-journal.net/online_features/health_and_wellness/article_a08ace44-0ce9-5931-99fe-dc515a3ca060.html

Finding Courage to Face Life by Using the CHRONDI Creed

APRIL 5, 2019 A COLUMN BY DR. C.

My previous eight columns addressed the CHRONDI Creed, a plan anyone can put in place when seeking to live better with a chronic disease. The CHRONDI Creed is challenging to put in place as a way of life. It takes courage to face life honestly and to make the changes needed to move toward well-being. It takes courage to wake up every day with a chronic disease and to stand tall with the CHRONDI Creed as your action plan.

Life is about choices. Using the CHRONDI Creed is a choice. I could say to myself, “I am tired of having to do all this hard work.” And on bad days, that voice gets annoyingly loud.

That voice was particularly loud while driving to my monthly doctor’s visit for my other chronic disease, ocular histoplasmosis. It’s an eye disease, and I need chemo treatmentinjected in the eye every month. This treatment is scary. Imagine watching a needle coming straight for your eyeball and then watching the fluid being injected. Imagine the thoughts and fears.

I sign a waiver every time because of the risks involved with this treatment. Do I want to want to do this? Dumb question, right? But if I don’t do it then there is a chance the disease will eventually take my sight. It’s a choice. I could choose not to do it, but instead, I choose to face this scary treatment every month. Courage is not the absence of fear, but rather facing fear and doing what promotes health.

It takes courage to use the CHRONDI Creed as a way of living better with a chronic disease. CHRONDI stands for the following:

C – Compassion: I will act compassionately toward others and find gentleness toward self.

H – Happiness: I will seek the inner bliss of happiness that is not material in nature.

R – Rehabilitation: I will apply courage and mindfulness to a total health rehabilitation plan.

O – Others: I will genuinely communicate with others about my experiences and maintain an attitude of gratitude for their help.

N – Nature: I will take time to embrace nature and all its beauty, which may include gardening, walks in the forest, and just sitting with nature.

D – Death: I will find the courage to face the terror of the “death of self” (loss) and not let it control me.

I – Individuality: I will continue to express my individuality and my purpose beyond the disease.

The CHRONDI Creed is a series of self-affirming statements. (For more detailed information about each one, click on the links above.) I start each day with these statements and have been doing so for years. They have become my inner dialogue — most of the time. It’s a healthy inner dialogue to replace all the negative, sometimes nasty, inner noise. Keeping that negative noise numbed down to a level of minimal impact is an important part of my personal plan for well-being.

Choosing to live by the CHRONDI Creed is not quite as intrepid as a needle stuck in your eye, but it is still something that takes a strong dose of courage. It takes courage to look honestly at your life and ask, “Am I living by this creed?”

I have found that the CHRONDI Creed gives me more strength, helps me to have more courage, and adds to my quality of life while living with a chronic disease. I am always looking for a way to live the creed more completely.

Where have you needed to draw upon courage in making choices to live better with a chronic disease? Please share in the comments below. 

***

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/2019/04/05/finding-courage-face-life-chronic-disease-using-chrondi-creed/

Phase 1/2 Trial to Test Investigational Therapy RTB101 in Parkinson’s Disease

 APRIL 5, 2019  BY PATRICIA INACIO, PHD 

A new Phase 1/2a clinical trial will investigate resTORbio’s therapy candidate RTB101,alone or in combination with sirolimus, as a potential treatment for Parkinson’s disease.

Researchers plan to enroll 45 patients with mild Parkinson’s disease, both with and without mutations in the GBA gene, and who are being treated with standard therapies.

The trial is intended to assess the safety and tolerability of RTB101 alone or in combination with sirolimus (sold under the brand name Rapamune, among others). The participants will be randomized into five groups where, with the exception of one group that does not receive RTB101, they’ll be given 300 mg of RTB101 once weekly either alone or combined with three escalating doses of sirolimus (2 mg, 4 mg, and 6 mg) or a matching placebo. Patients will be dosed for four weeks.

Its primary objective is safety and tolerability, and as secondary goal, researchers will measure the levels of RTB101 in the blood and the cerebrospinal fluid (CSF; the liquid surrounding the brain and spinal cord). Exploratory goals include measuring biomarkers in blood and CSF, and various clinical assessments. Data from the trial is expected in 2020.

“We believe that TORC1 may be an important therapeutic target for several neurodegenerative diseases associated with aging, in which misfolded proteins aggregate and cause neuronal toxicity. As such, we are excited to initiate our first clinical trial in PD and expand our pipeline into neurodegenerative disease,” Chen Schor, co-founder, president, and CEO of resTORbio, said in a press release.

Aging is the largest risk factor for the development and progression of Parkinson’s disease. In patients with the disease, a protein called the mechanistic target of rapamycin, or mTOR, is frequently over-activated in the brain, preventing the cells from reacting in a functional and timely manner to threats, such as the buildup of toxic forms of the alpha-synuclein protein.

mTOR is a central regulator of cellular growth, survival, and protein synthesis, among other processes. It works by regulating multiprotein complexes known as TORC1 and TORC2 (target of rapamycin complex 1 and 2).

In preclinical studies, inhibition of TORC1 prolonged the lifespan and enhanced several body functions, including immune responses, memory, and mobility, and delayed the onset of aging-related diseases in mice.

Proposed mechanisms for TORC1’s inhibition in Parkinson’s disease is linked to cells’ natural recycling system called autophagy. TORC1 is a natural inhibitor of autophagy. In the case of Parkinson’s disease, defective autophagy prevents the clearance of toxic protein aggregates such as alpha-synuclein.

Inhibiting TORC1 with the small molecule RTB101, alone or combined with sirolimus (an inhibitor of the master regulator mTOR), activates autophagy, promoting the clearance of these harmful protein aggregates. As a result, the treatment halts neuronal loss and improves motor function.

RTB101 has been shown to potently activate autophagy in the central nervous system (brain and spinal cord) and co-administration with sirolimus means that the concentration required for RTB101 to work is potentially lower — both therapies will act synergistically.

Caused by mutations in the GBA gene, impaired activity of the enzyme glucocerebrosidase (GCase), which is responsible for breaking down and recycling cell waste, has been linked to neurodegeneration and accumulation of alpha-synuclein in Parkinson’s disease. Treatment with RTB101 has also been shown to modulate the activity of GCAse.

“Multiple preclinical models of PD [Parkinson’s disease] have demonstrated the potential benefits of TORC1 inhibition, and intermittent TORC1 inhibition with a synergistic combination of RTB101 and sirolimus may serve as a promising approach for the treatment of PD. We look forward to reporting data from this trial in 2020,” Schor said.

https://parkinsonsnewstoday.com/2019/04/05/phase-1-2-trial-testrtb101-parkinsons/

Growing LRRK2 Protein Crystals in Space Could Help Scientists Better Understand and Treat Parkinson’s

APRIL 5, 2019 BY JOSE MARQUES LOPES, PHD

Crystals of the LRRK2 protein grown aboard the International Space Station could improve the understanding of Parkinson’s disease and help develop more effective therapies for this disease, according to researchers.

Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common genetic cause of Parkinson’s and result in excessive activation of the LRKK2 protein. Although treatments designed to block the LRRK2 protein are in development, the precise structure of this enzyme is still unknown, thereby limiting the likelihood of successful clinical trials.

One approach is to create crystals of LRRK2, but growing them on Earth is difficult and results in crystals without enough quality for researchers to determine the protein’s shape and structure. However, growing protein crystals in space — in microgravity conditions — makes them larger and more uniform, providing a way to better understand Parkinson’s. Such is the goal of the study, “Crystallization of LRRK2 Under Microgravity Conditions-2 (CASIS PCG 16).”

This investigation builds on a previous experiment known as CASIS PCG 7, which resulted in a study published in early 2018. Despite being able to successfully adapt the crystallization method to enable the transport of LRRK2 to the space station, scientists found that growing the protein crystals in microgravity did not improve their quality.

For this subsequent experiment, the space crew used larger sample wells, filled them during flight in the SpaceX Dragon capsule, and tracked the growth of the LRRK2 crystals, according to a NASA news release, written by Melissa Gaskill.

The crystals are then re-analyzed with techniques called x-ray diffraction and neutron diffraction upon return in a frozen state to Earth.

In an online video, NASA astronaut Serena Auñon-Chancellor narrates as Alexander Gerst, a European Space Agency astronaut, examines and photographs the LRRK2 crystals with a microscope. Gerst was able to interact in real time with researchers on the ground, who were at the Michael J. Fox Foundation, at Goethe University Frankfurt in Germany, and at the University of California San Diego.

According to the team, this project could also help advance the understanding of protein structure and boost interest in conducting research aboard the space station.

The investigation was sponsored by the International Space Station U.S. National Laboratory.

https://parkinsonsnewstoday.com/2019/04/05/growing-lrrk2-protein-crystals-space-help-scientists-better-understand-treat-parkinsons/

Researchers find probiotics may increase intestinal motility in mouse model

 by Janet Christenbury, Emory University April 5, 2019

Andrew Neish, MD. Credit: Emory University

Emory researchers have found that adding good bacteria into the intestines can guide the development of the enteric nervous system, also called "the gut brain," while increasing intestinal motility, or movement of the digestive tract, in a mouse model. The results are good news for medical conditions such as irritable bowel syndrome, Parkinson's disease, autism and others, where activity in the digestive tract is slowed. The findings were published in the journal Gastroenterology on March 28, 2019.

Andrew Neish, MD, professor of pathology and laboratory medicine at Emory University School of Medicine, is senior author on the Gastroenterology paper. Neish and researchers in his laboratory have been studying gut microbiota (bacteria in the intestines) for many years, primarily in regard to gut inflammation and infection in mouse models. But their research recently turned to gut motility. 

Gut motility is the contractions and relaxations of the muscles in the gastrointestinal (GI) tract, which controls and propels movement of food throughout the digestive tract. 

"A junior faculty member in the lab, Bindu Chandrasekharan, Ph.D., found that the mechanisms by which the gut microbiota influences inflammation may similarly also affect neural cells in the gut," says Neish. "This is important because if neurons in the enteric nervous system can perceive microbiota-derived components, we may also be able to regulate gut motility, or movement of the digestive tract, using probiotics." Chandrasekharan is first author on the paper.

To test their work, the researchers gave mice daily doses of probiotics (Lactobacillus rhamnosus GG) for one week. Then they collected and examined the intestinal tissues of the mice. They found the daily probiotics stimulated functional changes in the "gut brain". They also found that a one-week regimen of probiotics significantly increased stool frequency, reduced total GI transit time and increased contractions throughout areas of the GI tract, resulting in better food movement through the digestive tract in the mice.

"This data has clear implications for potential therapeutic plans to introduce specific bacteria into the gut that may increase gut motility," says Chandrasekharan. "Patients with diverse disorders including diabetes, autism, Parkinson's disease and irritable bowel syndrome often experience the common symptoms of compromised gut motility or constipation that adversely affect their quality of life."

"We hope these findings will eventually yield specific probiotic therapeutic approaches for the treatment of functional bowel or gut disorders in patients," says Neish.

More information: Bindu Chandrasekharan et al. Interactions Between Commensal Bacteria and Enteric Neurons, via FPR1 Induction of ROS, Increase Gastrointestinal Motility in Mice, Gastroenterology (2019). DOI: 10.1053/j.gastro.2019.03.045

Journal information: Gastroenterology 

Provided by Emory University 

https://medicalxpress.com/news/2019-04-probiotics-intestinal-motility-mouse.html

New ALS gene expression atlas offers unprecedented detail into disease progression

by New York Genome Center  April 4, 2019

Hemali Phatnani, PhD, Director of the New York Genome Center's Center for Genomics of Neurodegenerative Disease (CGND) and Silas Maniatis, PhD, Staff Scientist, CGND, (l to r) examine the multidimensional data available in the new ALS gene expression atlas, being made available to the research community via interactive exploration portal https://als-st.nygenome.org . Credit: New York Genome Center

ALS researchers at the New York Genome Center (NYGC) have utilized new technologies for mapping gene expression in spinal cord samples that provide new insights into the mechanisms that contribute to disease onset and progression in ALS patients.

In a global collaboration that included scientists at the Simons Foundation's Flatiron Institute in New York, the Science for Life Laboratory and KTH Royal Institute of Technology in Sweden, and New York University, researchers at the NYGC's Center for Genomics of Neurodegenerative Disease (CGND) used spatial transcriptomics, combined with a novel computational approach, to obtain gene expression measurements over time and space for close to 12,000 genes in the spinal cord. The result is a new, multidimensional gene expression atlas, providing unparalleled detail and scale and offering a previously unavailable view of disease progression in ALS.

In a new study in Science, the researchers describe how the spatiotemporal gene expression atlas uncovers early changes in ALS disease not observable using traditional sequencing methods. The scientists also developed novel computational approaches that reveal disease-driven changes in the activity of many signaling pathways across all cell types in the central nervous system, which may reveal novel targets for designing therapeutics and diagnostics.

What makes this study unique from previous transcriptome profiling research is the method used by the scientists, Spatial Transcriptomics, which generates RNAseq profiles at many locations in a tissue section simultaneously. Thus, the team was able to record precisely where in the tissue virtually every gene is expressed. The researchers examined four time points during disease progression, from earliest adulthood to end stage in a mouse model of ALS. In addition, postmortem spinal cord samples from ALS patients were examined.

"Spatial Transcriptomics allows us, for the first time, to gain important insights into gene expression in individual cell types while in their natural multicellular context," explained Hemali Phatnani, Ph.D., Director of NYGC's CGND, senior author of the study. "It enables unprecedented interrogation of cell-to-cell interactions so that we can now examine and explore specific pathways in ALS where things are going wrong, where and in which cell types dysfunction is first seen, and how this spreads through the spinal cord."

The scientists have made this multidimensional gene expression atlas available as a resource to the research community via the interactive data exploration portal. They believe that the study can provide a framework for further mapping of the central nervous system and its modes of dysfunction, to aid research into not just ALS but also other neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.

A relatively new method enables researchers to study tissue samples in high resolution to determine where genes are expressed. In these four cross-sections of a mouse spinal cord, each dot represents an individual measurement site. Yellower dots represent regions with elevated expression of the CHODL gene. Credit: S. Maniatis et al./Science 2019

The ongoing insights to be gleaned from this comprehensive, spatiotemporal, transcriptome-wide gene expression dataset will be crucial to advancing understanding of ALS, a complex neurodegenerative disease with no clear cause or known cure. More than 200,000 people worldwide are living with ALS, also known as Lou Gehrig's disease, which typically manifests at first in distal muscles of a single limb, and then spreads throughout the body, leading to total paralysis and death. The average life expectancy of a person with ALS is about two to five years from the time of diagnosis.

In their paper, "Spatiotemporal Dynamics of Molecular Pathology in Amyotrophic Lateral Sclerosis," the team collected 76,136 spatial gene expression measurements (SGEMs) from 1,165 mouse tissue sections and 61,031 SGEMs from 80 human tissue sections (for context, the next largest comparable spatially resolved transcriptomics studies considered only about a dozen tissue sections at a single time point). By combining the data from many tissue sections, the researchers were able to detect the expression of close to 12,000 genes simultaneously across the tissue region under examination. This is the first time that such a spatially resolved approach has been used to study ALS at this depth and scale.

"Even though it is the motor neurons that are most vulnerable in ALS, the neighboring cells that surround the motor neurons also play a role in the disease," said co-first author, Silas Maniatis, Ph.D., Staff Scientist at NYGC's CGND. "Our research focuses on understanding how disease-causing mutations disrupt the function of both neuronal and non-neuronal cells, and how disrupted interactions between the various cell types of the nervous system drive motor neuron loss in ALS. Spatial Transcriptomics and the associated computational tools we developed in this study give us a superb view of these processes. Perhaps more importantly, this combination of technologies and experimental approaches provide a framework for understanding other diseases of the nervous system."

TYROBP, a gene linked to ALS, lights up across a thin cross-section of spinal cord tissue from a person with ALS. Expression of the gene is elevated in some regions (yellower dots), a new study shows. Credit: S. Maniatis et al./Science 2019

Corresponding authors on the study include: Joakim Lundeberg, Ph.D., whose lab developed the Spatial Transcriptomics method, and is head of the department of Gene Technology at the KTH Royal Institute of Technology, and Director of the Genomics platform at SciLifeLab, an institution for the advancement of molecular biosciences in Sweden; and Richard Bonneau, Ph.D., Professor of Biology, Computer Science, and Data Science, New York University, and Group Leader for Systems Biology at the Center for Computational Biology at the Simons Foundation's Flatiron Institute, who led the team in devising novel computational methods for analysis of atlas data.

"The study is a beautiful example that 'geography' matters, i.e., being able to spatially position subtle gene activity changes and linking these to initial steps in the disease. An added benefit is that information is indeed provided in a data-driven manner using the wealth of information provided by transcriptome-wide technologies in situ," said Dr. Lundeberg.

"The synergy of this global collaboration has resulted in the development of a powerful new genomic tool that provides researchers with a wealth of information in a data-driven manner," said Dr. Bonneau.

More information: "Spatiotemporal dynamics of molecular pathology in amyotrophic lateral sclerosis" Science (2019). science.sciencemag.org/cgi/doi … 1126/science.aav9776

An interactive data exploration portal is publicly available at http://als-st.nygenome.org/.

Journal information: Science 

https://medicalxpress.com/news/2019-04-als-gene-atlas-unprecedented-disease.html

Parkinson's clues seen in tiny fish could aid quest for treatments

by University of Edinburgh  April 4, 2019

Research using zebrafish has revealed how key brain cells that are damaged in people with Parkinson's disease can be regenerated. In this microscope picture of a zebrafish brain, dopamine-producing nerve cells are shown in red and the stem cells that produce them are shown in green. Credit: Thomas Becker, The University of Edinburgh

Parkinson's patients could be helped by fresh insights gained from studies of tiny tropical fish.

Research using zebrafish has revealed how key brain cells that are damaged in people with Parkinson's disease can be regenerated.

The findings offer clues that could one day lead to treatments for the neurological condition, which causes movement problems and tremors.

Parkinson's occurs when specialised nerve cells in the brain are destroyed. These cells are responsible for producing an important chemical called dopamine.

When these cells die, or become damaged, the loss of dopamine causes body movements to become impaired. Once these cells are lost from the human brain, they cannot be repaired or replaced.

In zebrafish, however, dopamine-producing nerve cells are constantly replaced by dedicated stem cells in the brain, the researchers found.

The team, led by the University of Edinburgh, found the immune system plays a key role in this process. In some regions of a zebrafish's brain, the process does not work, however.

Researchers say understanding the immune signals that facilitate replacement of these nerve cells could hold vital clues to developing treatments for people.

The study, published in the Journal of Neuroscience, was funded by the Biotechnology and Biological Sciences Research Council and the Medical Research Council.

Dr. Thomas Becker, of the University of Edinburgh's Centre for Discovery Brain Sciences, said: "We were excited to find that zebrafish have a much higher regenerative capacity for dopamine neurons than humans. Understanding the signals that underpin regeneration of these nerve cells could be important for identifying future treatments for Parkinson's disease."

More information: Journal of Neuroscience (2019). DOI: 10.1523/JNEUROSCI.2706-18.2019

Journal information: Journal of Neuroscience 

https://medicalxpress.com/news/2019-04-parkinson-clues-tiny-fish-aid.html