See the world through Robert Flatt’s lens

Friday, August 16, 2019  By Rebecca Maitland, Correspondent  

Robert Flatt’s book, Healing Art — Don’t Let Anything Ruin Your Day

It is never too late to start a new hobby, or to take up a silent passion you’ve had for a long time, and one person who is a living example of this, is Robert Flatt, 71, an engineer, photographer, philosopher and author. Flatt is also fighting Parkinson’s disease.

Robert Flatt

“Eventually you will have bodies like mine that do not work very well (from the disease of aging). Eventually you’ll no longer be able to do your current job, and this will give you a marvelous gift — the gift of time. You can squander this gift by sitting around feeling sorry for yourself, or you can try to find something interesting to do, with whatever physical ability you have left. Once thing, you will certainly have time for is to be happy, which is often called smelling the roses — though you may not be able to physically smell or even see or touch a real rose,” Flatt said

After being an engineer in the oil service industry for 31 years, and after being diagnosed with Parkinson’s disease, Robert Flatt retired in 2004. It was not long until he immersed himself in his hidden passion of photography.

Flatt and his wife met when they were 15, attended college together at Rice University and have been married for 50 years. The couple loves to travel, and when they were hiking in Olympic National Park, Flatt noticed that his backpack kept tilting. He thought he needed new equipment, but is was Parkinson’s.

So, after being an engineer in the oil service industry for 31 years, and after being diagnosed with Parkinson’s disease, he retired in 2004. It was not long until he immersed himself in his hidden passion of photography, taking every class there was to take at Rice.

After photography classes, Flatt and his wife spent many years traveling the world, mainly for the purpose of allowing him opportunities to capture exquisite images of the wonders of nature.

Flatt is now an acclaimed photographer, and his photos are featured in a permanent exhibit at Baylor University Department of Neurology and the Museum of Fine Arts, Houston. Rice University also awarded him with the Gold Medal for Meritorious Service. He has authored a photographic journal filled with breathtaking images, and his life lessons and perspectives on life and photography.

“I have written and published a book about my 15-year battle with Parkinson’s disease, Healing Art — Don’t Let Anything Ruin Your Day. The subtitle refers to how we have a chance to defeat debilitating diseases like Parkinson’s. We can’t change the fact that we have the disease, but we can, by God, not let it ruin our day today — maybe tomorrow, but not today,” Flatt said.

On one of the pages from his book, with a hummingbird featured, he writes, “I believe that to get one of those really great photographs, you’ve got to somehow shut down the rational, sobering brain and listen only to your heart.

“An opportunity for a really great photograph, or any photograph, only exists for a brief moment in time. If you miss it, you don’t just miss it for today, but you miss it for all eternity. To rephrase Sir Francis Bacon: ‘Take the picture now. You will not get another chance. There is no rewind button.’”

One of the things Flatt hopes people will take away from his book, which can be purchased from most bookstores and online, is that he believes life is good, that beauty is all around us, though we have to look for it.

And that we need to live as much as possible in the present and know that time is precious. After all, there is no rewind button.

Today, Flatt and his wife are residents at Brazos Towers at Bayou Manor, enjoying the community, giving talks on his book, and he is still taking photos.

“Parkinson’s disease gave me the gift of time to learn to take photographs that hopefully will give you some peace, joy, love and laughter. So, the book is full of the best pictures I have taken over the last 10 years combined with text about the ways that I have tried to cope with my disease,” Flatt said.

https://www.chron.com/news/article/See-the-world-through-Robert-Flatt-s-lens-14335429.php#photo-18103276

Info session coming Aug. 23 on how exercise can help Parkinson's patients

August 16, 2019

Justin Waller, Granville County senior services' fitness program coordinator, is shown with Clarence Lemons, Phyllis Paschall, Nancy Cordin and Phyllis Russell in an exercise session at Granville Athletic Park earlier this year. Submitted photo

OXFORD For those living with Parkinson's disease, exercise can help reduce stiffness and improve mobility. Join Justin Waller, Granville County senior services fitness program director, for an informational session on Friday, Aug. 23, to learn how exercise can be an adjunct treatment for Parkinson's. The session will be held at 2 p.m. at the Granville County Senior Center in Oxford.

https://hendersondispatch.com/news/4805/info-session-coming-aug-23-on-how-exercise-can-help-parkinsons-patients/

Using math to help treat Alzheimer's, Parkinson's and other diseases

AUGUST 16, 2019   by Leah Burrows, Harvard University

Illustration of protein aggregation. Aggregates are formed through an initial primary nucleation step followed by elongation. Once a critical concentration of aggregates is reached, secondary nucleation introduces a positive feedback cycle leading to exponential growth of aggregate concentration. Credit: L Mahadevan/Harvard SEAS

Protein aggregation—in which misfolded proteins clump together to form large fibrils—has been implicated in many diseases including Alzheimer's, Parkinson's, and type II diabetes. While the exact role these fibrils play in diseases isn't fully understood, many of the current treatments for diseases like Alzheimer's and Parkinson's target the aggregation process. However, finding the right treatment protocols for these drugs, which can be toxic in large doses, is challenging.

Recently, researchers from the Harvard John A. Paulson School of Engineering and Applied Sciences (SEAS) developed a model to better understand how drugs inhibit the growth of protein fibrils, offering a guide to develop more effective strategies to target protein aggregation diseases. The researchers found that different drugs target different stages of protein aggregation and the timing of their administration plays a critical role in inhibiting fibril growth.

"Our research highlights the importance of understanding the relationship between the chemical kinetics of protein misfolding, the mechanisms by which drugs inhibit protein aggregation, and the timing of their administration," said L Mahadevan, the Lola England de Valpine Professor of Applied Mathematics, of Organismic and Evolutionary Biology, and of Physics at Harvard University. "This understanding could have important implications for intervention protocols to prevent pathological protein aggregation."

Protein aggregation involves a number of steps, beginning with what's called primary nucleation, in which the misfolded proteins join together to form a fibril, which then elongates. Once a critical number of fibrils is formed, aggregation accelerates due to a process known as secondary nucleation, leading to exponential growth. The first step associated with the formation of the fibrils is very slow, typically taking several decades, which could explain why Alzheimer's often affects people in their old age. However, once those first fibrils are formed, the disease can progress very rapidly.

Using mathematical methods from control theory, combined with the physics of protein aggregation, the researchers made theoretical predictions on how and when to intervene using drugs.

To test their results, the researchers looked at previously published data on the efficacy of drugs in a model organism, the round worm, C. elegans, where one can trigger the formation of Amyloid b, a misfolded protein associated with Alzheimer's disease. Its treatment is carried out using two compounds that inhibit the formation of Amyloid b: Bexarotene and DesAb29-35.

The researchers found that drug efficacy depends on whether the compound inhibits primary nucleation or secondary nucleation. Bexarotene, for example, selectively inhibits the primary nucleation that happens early in the disease while DesAb29-36 inhibits secondary nucleation that happens later. 

In the absence of drugs, Amyloid-b aggregation causes paralysis in the worms. When Bexarotene was given at the onset of the disease in the larval stages, published data shows that there was a significant recovery of the worm's mobility. The data also showed that DesAb29-36 was more effective when administered later in the disease's progression.

"By combining well-known concepts from two different fields, the kinetics of protein aggregation, and optimal control theory, we linked molecular-scale phenomena to macroscale strategies with relevance for a real, practical problem," said Mahadevan.

"Our approach, which draws on a detailed understanding of the aggregation process and uses this understanding to design rationally potential strategies, is unique," said Thomas C. T. Michaels, a postdoctoral fellow at Harvard and co-first author of the study along with Christoph Weber, who was a postdoctoral fellow at Harvard and is now a junior group leader at the Max Planck Institute for Complex Physical Systems in Dresden, Germany. "It will allow people to test the efficacy of different compounds against aggregation under optimal conditions at the drug discovery and drugscreening level. From these optimal conditions, one could then extrapolate optimal conditions for a trial. So, in this sense, our work could help seed potential trials."

The research was published in the Proceedings of the National Academy of Sciences.

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More information: Thomas C. T. Michaels et al. Optimal control strategies for inhibition of protein aggregation, Proceedings of the National Academy of Sciences (2019). DOI: 10.1073/pnas.1904090116

Journal information: Proceedings of the National Academy of Sciences 

Provided by Harvard University 

https://medicalxpress.com/news/2019-08-math-alzheimer-parkinson-diseases.html

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

AUGUST 16, 2019 Dr. C

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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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/2019/08/16/heat-intolerance-weather-symptoms/

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

 AUGUST 15, 2019    BY PATRICIA INACIO, PHD 

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

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

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

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

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

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

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

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

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

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

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

https://parkinsonsnewstoday.com/2019/08/15/parkinsons-uk-awards-scientist-100000-grant-identify-ways-protecting-dopamine-producing-neurons/

The Parkinson’s Foundation launches large-scale genetic study, aiming to improve patient care and speed clinical trials

By Samantha Black, Ph.D.  August 14, 2019 

More than 10 million people worldwide are currently living with Parkinson’s disease (PD), a neurodegenerative disorder that impacts the dopamine-producing neurons in the brain. Scientists do not know exactly what causes PD, but they believe it is a combination of genetic and environmental factors. Nearly 10% to 15% of all PD cases are caused by genetic mutations. A new study aims to understand how the disease develops and how it can be treated or cured. This study, target="blank">PD GENEration: Mapping the Future of Parkinson’s Disease is currently being conducted by the Parkinson’s Foundation.

Dr. James Beck

On August 9, 2019, The Science Advisory Board had the pleasure of discussing PD GENEration with James Beck, PhD, Chief Scientific Officer of the Parkinson’s Foundation. The study is a first-of-its-kind initiative that offers free genetic testing for clinically relevant Parkinson’s related genes and free genetic counseling for patients to help them better understand their results.

The goals of this program are threefold. First, the Parkinson’s Foundation hopes to empower those with Parkinson’s Disease (PD) to learn whether they have a genetic form of the disease. Secondly, the study will help the PD community enter an era of precision medicine, which is becoming an increasingly important tool for clinicians. And lastly, according to Dr. Beck, this program offers a pragmatic approach that not only enables clinicians to be able to provide the right type of care, but also one that will help companies identify new therapies in the pipeline and subsequently expedite clinical trials for PD patients.

The Parkinson’s Foundation will collaborate with a number of institutions to power this study, which is available to anyone with PD and will be offered through the Parkinson’s Foundation Centers of Excellence network and Parkinson Study Group sites. Parkinson’s Foundation Centers of Excellence are medical centers with specialized teams of neurologists, movement disorder specialists, physical and occupational therapists, mental health professionals and others who are up to date on the latest PD medications, therapies and research to provide the best care. Parkinson Study Group is a non-profit group of physicians and other health care providers from medical centers in the United States, Canada and Puerto Rico experienced in the care of PD patients and dedicated to clinical research of PD. The Centers of Excellence include over 48 medical centers around the world, and Parkinson Study Group consists of a network of 132 credentialed PD Centers across North America. According to Dr. Beck, the collaboration with Parkinson Study Group “doubles [the study’s] footprint in the US.”

The Parkinson’s Foundation is partnering with Fulgent Genetics to process, sequence and store DNA samples. High quality genetic testing through clinicians provide unique set of genetic test tailored to PD. PD genes are not always easy to sequence, and Fulgent has been successful where other companies have failed. Fulgent, in collaboration with the Parkinson’s Foundation, has developed a targeted list of seven genes (GBA, LRRK2, SNCA, PRKN, PARK7, VPS35, and PINK1) relevant to PD to sequence for the study.

Dr. Beck discussed how these seven genes were selected:

“LRRK2 and GBA are the two genes where clinical development is furthest along in pharmaceutical companies. More than a half dozen companies have small molecules in development that will target these genes as potential therapies for PD, that’s clear. The remaining five are interesting because we’ve had long discussions with our steering committee and a lot of input to come up with these. But they are really the ones that are relevant to PD and potential therapies coming down the pipeline. These remain interesting targets for drug companies. But they are also the ones that are distinctly relevant and easily identified when it comes to PD. These are probably the seven most common genetic forms of PD. They drop off dramatically after LRRK2 and GBA, but they’re worthwhile to identify nevertheless. There is real interest in how they may be potential targets for future clinical trials. We are not there yet, but there has been discussion, certainly in the literature, that at some point each one has a potential therapeutic target.”

Fulgent will use state-of-the-art next generation sequencing technology to analyze the DNA samples. Dr. Beck states that Fulgent is a unique partner because they have a powerful bioinformatics pipeline, with rigorous computational tools to analyze data in a meaningful way.

Advancing clinical therapies is a key aim of the PD GENEration study in addition to empowering patients to identify if they have a genetic form of PD, then enroll in clinical trial for new therapies. Previously, genetic testing allowed Parkinson’s patients to determine if they had a LRK2 or GBA mutation, but there was no direction, guidance or next step to be followed using this information. Now, “there is something to be done” says Dr. Beck. “If people know they have a genetic form of Parkinson’s Disease then they are more likely to enroll in clinical trials that they can see benefit from.”

There are several pharmaceutical companies that have PD therapeutics in their pipelines. Currently, Sanofi has a substrate inhibitor, venglustat, in phase II trials, and Denali Therapeutics has a LRRK2 inhibitor small molecule, DNL201, in phase I testing. The Parkinson’s Foundation hopes that by helping patients identify if they have a genetic form of the disease, and encouraging them to enroll in clinical trials, the development timeline for various therapies, such as venglustat and DNL201, will be greatly accelerated.

The data collected from this study will be a crucial tool for drug discovery and disease research moving forward. Banking the DNA of participants allows for the potential of whole genome sequencing in the future. This will allow researchers to identify unique factors that can play a role in PD. According to Dr. Beck, the Parkinson’s Foundation plans to make the data available to researchers and clinicians in the future so that they can learn more about how genetics impact PD.

The hope is to make the data available for qualified researchers in about six months’ time, as the genetic analysis is just starting to roll into their systems now. For scientists the data will be made available through a portal on the Parkinson’s Foundation website and will be updated regularly with the latest data. If you are interested in working with this data, the Parkinson’s Foundation provides a number of funding opportunities with a focus on early career investigators. As the CSO, Dr. Beck appreciates the processes involved in research. “I can use that to guide how we approach funding and recognize the career structure of a scientist. I can understand the pain points and identify where support from an outside entity may be really helpful.”

Dr. Beck is a passionate professional who believes that working towards understanding the science behind PD and unique populations of patients will ultimately enable researchers to develop new therapies and equip clinicians with the information they need to provide the best care possible. He also stressed the importance of supporting young scientists who are passionate and want to study PD. His background in teaching and science communication has followed him to his current role where he supports programs that provide opportunities for young scientists to hone their communication skills.

The PD GENEration study is going to provide a more comprehensive understanding of PD for the community and help PD patients globally. The Parkinson’s Foundation is actively seeking industry partners to provide feedback as this study progresses and wants to provide something to the community as a whole. As Dr. Beck suggests, the future of PD will be “precision guidance tailored to someone’s specific disease” and this study will move us one step closer to that goal.

If you have any additional questions about the PD GENEration study or would like to find out more about the Parkinson’s Foundation please visit www.parkinson.org.

https://www.scienceboard.net/index.aspx?sec=ser&sub=def&pag=dis&ItemID=225

New technology could aid stem cell transplantation research

14-Aug-2019      Rutgers University

Caption

Nanotechnology developed at Rutgers University-New Brunswick could boost research on stem cell transplantation, which may help people with Alzheimer's disease, Parkinson's disease, other neurodegenerative diseases and central nervous system injuries. The scientists' nanotechnology platform uses special tiny rods with nickel and gold to detect microRNA inside exosomes. Exosomes - tiny particles released by cells that play a critical role in cell-to-cell communication - are next generation biomarkers. The scientists successfully monitored the generation of neurons from human stem cells by characterizing exosomes without destroying them. The efficient technology can also be used to characterize heterogeneous brain tissue.

Credit

Jin-Ho Lee/Rutgers University-New Brunswick

   

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Nanotechnology developed at Rutgers University-New Brunswick could boost research on stem cell transplantation, which may help people with Alzheimer's disease, Parkinson's disease, other neurodegenerative diseases and central nervous system injuries.

The nanotechnology platform, which uses special tiny rods for sensing, allows researchers to confirm the identity of human stem cell fates and their biomarkers, or biological molecules, without destroying them, according to a study in the journal ACS Nano. That's been a major issue during pre-clinical research on stem cells because it limits further analyses and biomedical applications.

"One of the major hurdles in the current cell-based therapies is the destructive nature of the standard cell characterization step. With our technology, we can sensitively and accurately characterize the cells without compromising their viabilities," said senior author KiBum Lee, a professor in the Department of Chemistry and Chemical Biology in the School of Arts and Sciences.

Stem cells can develop into many different types of cells, including neurons that transmit information in the brain. Adult human-induced pluripotent stem cells, which resemble embryonic stem cells, can be used to develop drugs and model diseases, according to the National Institutes of Health. Scientists hope to use them in transplantation medicine.

While stem cells hold great potential for treating neurodegenerative diseases and central nervous system injuries, controlling and characterizing their fate are critical issues that need to be addressed before their potential use as treatments can be fully realized. Current methods for characterizing stem cell biomarkers destroy cellular activities and functions, which makes it difficult to conduct more definitive research that could lead to biomedical applications.

Using their nanotechnology platform, the scientists successfully monitored the generation of neurons from human stem cells by characterizing next generation biomarkers called exosomes - tiny particles released by cells that play a critical role in cell-to-cell communication. The scientists will further investigate their technology's versatility in other applications, such as detecting neurons in clinical settings.

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Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

https://www.eurekalert.org/pub_releases/2019-08/ru-ntc081319.php

Nexeon Medsystems explores where technology and the nervous system intersect

Anne Stych    Aug 13, 2019

Nexeon Medsystems is a finalist in the Emerging Company Innovation Award category for the 2019 Tech Titan awards. Category winners will be announced at an awards event on Friday, Aug. 23. 

For more information about the awards event, go to:  https://techtitans.org/awards-gala/

Nexeon Medsystems, Inc. CEO Will Rosellini

Nexeon Medsystems (OTC: NXNN) is a medical device company that’s exploring new ways to use established technology to fight diseases in a different way — someday that could mean integrating information sources directly into your nervous system.

One of Nexeon's advancements involves using pacemakers to interface with the nervous system and change the incorrect signals that diseases send to the brain into healthy signals.

For example, patients who have Parkinson's Disease often exhibit shaking as a symptom. Nexeon’s device intercepts the “bad” signals that are triggering the tremor and instead sends back the right information for the nervous system to use.

Chairman and CEO Will Rosellini responded to the Business Journal's questions about working in tech in DFW.

How would you define the intersection of people and technology?

People have a lot of trouble putting down their iPhone, and it's our belief that the information contained in the supercomputer that is your iPhone will someday be integrated into your nervous system directly. We've seen signs of this cyborg-level technology already in our lives, so if you're trying to not look at your phone while I'm talking, you understand why this technology is more likely to happen than not.

What’s an example of technology that people don’t use any more, and we take its replacement for granted?

My young children have a very difficult time understanding what cash is. As I try to explain, I find it hard to do. They look at my phone, and say “that's cash,” and I try to explain that it’s connected to paper money at the bank. Paper money is a very difficult concept to explain to kids today.

What is your biggest challenge as a company?

As a small, publicly-traded company, we struggle to explain a difficult science and engineering story to the retail investing public.

What do you think is something that will be an important technology in the future that people don’t see coming?

By 2027, fundamental characteristics of cell phone technology and the nervous system are going to astound people in terms of how much can be done with implantable devices. When you add in the influence of the internet of things, you’re going to have dramatic advances in the ways humans interact with computers.

https://www.bizjournals.com/dallas/news/2019/08/13/nexeon-medsystems-will-rosellini.html

Parkinson’s linked to gene on Y-chromosome in men for first time

August 14, 2019

Dr Joohyung Lee 

Parkinson’s disease (PD) is a progressive neurodegenerative disorder primarily associated with an inability to initiate and control voluntary movement.

The onset of Parkinson’s disease is caused by a loss of dopamine neurons in the midbrain. While it is unknown what causes this neuron loss, being male has always been linked as one of the strongest risk factors to developing the disease.

Men are twice as likely to develop PD as women and the progression of the disease is more rapid in men. Traditionally, sex differences in PD have been attributed to the protective actions of estrogen in females.

However, the finding of this pre-clinical study by Dr Joohyung Lee and Professor Vincent Harley, published in the prestigious Proceedings of the Natural Academy of Sciences, show for the first time that a gene called SRY on the male Y chromosome exacerbates risk factors as well as disease progression in males.

Remarkably, the researchers found that when they lowered the expression of the SRY gene by using synthetic gene therapy, they found reduced dopamine neuron loss and diminished motor symptoms in males.

Their study is a world first in identifying a male-specific therapeutic target for a neurological disease.

Prof Harley said, “Currently, PD therapies only treat symptoms and do not halt or slow the disease.

“Male and female brains are different at all levels: molecular, cellular and behavioural. That’s why we believed it was important to explore potential sex genetic related causes of the disease,” he said.

Study findings

Professor Vincent Harley

In adult males, the SRY gene controls how the brain functions. SRY proteins regulate the synthesis of dopamine which controls voluntary movement.

The research team led by Dr Lee and Prof Harley found that males with PD produced an abnormally high amount of the SRY protein in their mid-brain.

Dr Lee said, “In the healthy adult male brain, the SRY gene functions to control dopamine neurons and dopamine synthesis. However, we think that in cases of PD, when the male brain starts losing dopamine neurons, the SRY gene tries to compensate by producing more dopamine.

“This over production of dopamine exacerbates inflammation in the male brain,” he said.

The findings suggest that supressing the SRY gene with therapy represents a new sex-specific strategy to slow or prevent dopamine loss for men affected with PD, which would slow down PD progression in men.

Next steps

Dr Lee said, “The next steps in progressing this finding would be to test a range of synthetic gene therapies on human cell culture models. Once we find the most effective therapy, we would then design a novel way to administer the therapy to patients.

“This is a very exciting step towards minimising PD in males,” he said.

Prof Harley said, “We hope our study excites interest in developing SRY-based inhibitors for men with PD.”

Facts: the SRY gene

• At the embryonic stage, the SRY gene initiates male-sex determination by directing the development of the gonads to testes, rather than ovaries.
• In adult human males, the SRY gene is also expressed in non-reproductive tissues, such as the heart, adrenal glands, kidneys and brain.
• The SRY regulates the creation of dopamine neurons which controls voluntary movement.

Collaborators:

University of California, Los Angeles

Funders:

Victorian Government’s Operational Infrastructure, Support Program, Australian NHMRC, CASS foundation, Rebecca L. Cooper Foundation, Helen McPherson Smith Trust and National Institute of Health (NIH) USA.

https://www.miragenews.com/parkinson-s-linked-to-gene-on-y-chromosome-in-men-for-first-time/