Our bodies do a lot on autopilot — breathing, keeping our hearts going, sweating, digesting our food. But sometimes those automatic functions don’t work automatically. 
So-called “autonomic dysfunction” is when that process, controlled by the autonomic nervous system, goes haywire.
23andMe’s new lead scientist for our Parkinson’s Research program, Lucy Norcliffe-Kaufmann, Ph.D., has been fascinated by that process since studying physiology for her doctoral degree at the University of Leeds.
In particular, Lucy was intrigued by fainting, which is a reflexive response triggered by the autonomic nervous system. In some cases, neurodegenerative conditions like Parkinson’s disease can damage or destroy a person’s autonomic nerves. So for some of those with Parkinson’s-related autonomic dysfunction, which among other things causes hypotension, characterized by a sudden drop in blood pressure upon standing. 
Lucy has continued to study this process throughout her career as a clinical autonomic neuroscientist. She spent several years as the associate director of<a href="https://med.nyu.edu/departments-institutes/neurology/divisions-centers/autonomic-disorders"> New York University’s Langone Health’s Dysautonomia Center</a>, also serving as an associate professor of neurology, neuroscience, and physiology there. Most recently she worked in the private sector with Theravance, where she worked on potential treatments for hypotension, a common problem among those with Parkinson’s disease.
Her role at 23andMe marks a new chapter in her career but also a continuation of this focus on conditions related to Parkinson’s. Along with this continued attention on neurodegenerative conditions, Lucy has always put patients at the center of her work. It’s that and the richness of 23andMe’s data that drew her to 23andMe, and its groundbreaking Parkinson’s research program.
We recently sat down with Lucy virtually to talk to her about her work, Parkinson’s disease, and what she’ll be focused on at 23andMe. Her responses below have been edited for length.
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 <figure class="wp-block-image size-large is-style-default"><img loading="lazy" decoding="async" width="679" height="1024" src="https://blogcms.23andme.com/wp-content/uploads/2022/03/Lucy_N-K-679x1024.jpg" alt="" class="wp-image-29636" srcset="https://blogcms.23andme.com/wp-content/uploads/2022/03/Lucy_N-K-679x1024.jpg 679w, https://blogcms.23andme.com/wp-content/uploads/2022/03/Lucy_N-K-199x300.jpg 199w, https://blogcms.23andme.com/wp-content/uploads/2022/03/Lucy_N-K-768x1158.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2022/03/Lucy_N-K-583x880.jpg 583w, https://blogcms.23andme.com/wp-content/uploads/2022/03/Lucy_N-K-782x1180.jpg 782w, https://blogcms.23andme.com/wp-content/uploads/2022/03/Lucy_N-K.jpg 1043w" sizes="auto, (max-width: 679px) 100vw, 679px" /></figure>
 
<h6>What inspired you to become a scientist?</h6>
My father died of diabetes and renal failure very young. I wanted to understand diseases and make a difference. That set me on the path of clinical research. 
<h6>Why did you focus your work on autonomic disorders and neurodegenerative diseases?</h6>
My Ph.D. focused on fainting, which is a reflex response triggered by the autonomic nervous system. Sometimes we would see patients with neurodegenerative diseases that destroy the autonomic nerves. After finishing my degree, I became more involved with patients who have neurological diseases and permanent malfunctioning of the autonomic nervous system that causes near-fainting each time they stand. 
<h6>During your time at NYU, your research included a lot of work directly with patients and advocacy groups. Why is that important in disease research? </h6>
It’s important that we listen to the patient community to find out what’s most bothersome for those living with diseases so that our research is targeting something relevant. The patient community also needs to be aware of what research opportunities are out there, so they can make a choice whether they want to participate. Finally, I think it’s important to close the loop so that patients and caregivers can understand how the research developments translate back to their care. Patients and caregivers are a critical part of our research success. They need to be with us every step of the way. 
<h6>Both at New York University and then I think when you were doing work at Theravance, you began doing more work related to genetics but also in the development of treatments. Can you explain a little about that? </h6>
At NYU, I was incredibly fortunate to spend 15-years working with a community of patients with familial dysautonomia, which is a rare Jewish genetic disease that affects the development and survival of the nervous system. These children are born without the ability to feel pain or temperature and regulate their blood pressure. When I joined NYU, familial dysautonomia was misunderstood from a neurological basis. Over the years, we helped understand what was the specific pattern of nerve loss that caused the symptoms, we partnered with the FDA’s Office of Orphan Product Development to find new therapies to treat the debilitating symptoms and worked on developing potential genetic therapies to help stop the ongoing neurological decline. This patient community shaped my research career, and for that, I will always be grateful. 
At<a href="https://www.theravance.com/"> Theravance</a>, I spent a year in industry working on developing a drug to treat orthostatic hypotension, which is a problem around 40 percent of patients with Parkinson&#8217;s disease develop due to their blood pressure falling to low levels when they stand. 
<h6>What are the kinds of scientific questions or problems you are drawn to?</h6>
I’m drawn to the types of questions that don’t have easy answers. I love clinical research that comes from following the patients and observing trends or patterns that teach us about diseases. I find clinical data fascinating because it comes from the patients. It’s their story and it’s up to us to think about what that means and how we can apply our knowledge to understand and develop better treatments. 
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 <figure class="wp-block-image size-large is-style-default"><img loading="lazy" decoding="async" width="861" height="916" src="https://blogcms.23andme.com/wp-content/uploads/2022/03/PD-Research.png" alt="" class="wp-image-29642" srcset="https://blogcms.23andme.com/wp-content/uploads/2022/03/PD-Research.png 861w, https://blogcms.23andme.com/wp-content/uploads/2022/03/PD-Research-282x300.png 282w, https://blogcms.23andme.com/wp-content/uploads/2022/03/PD-Research-768x817.png 768w, https://blogcms.23andme.com/wp-content/uploads/2022/03/PD-Research-827x880.png 827w" sizes="auto, (max-width: 861px) 100vw, 861px" /></figure>
 
<h6>What prompted you to come to 23andMe, and what specifically interests you about the Parkinson’s research program? </h6>
I really like the idea that 23andMe is following research participants with Parkinson&#8217;s disease. I’ve worked all my career in doing natural history studies. A big draw for me was the idea that we will be keeping in touch with these patients so we can understand how they evolve and we can link that back to genetics. You can only do so much when you see a patient once. But when you follow them over time you can understand much more. It’s this part that intrigues me. Each patient is a story that contributes to our understanding of Parkinson&#8217;s disease over time. Patterns start to emerge and that can change our understanding of neurological disease. 
<h6>Could you explain a little bit about what you’ll be doing in this new job?</h6>
I’ll be working within the Parkinson&#8217;s disease program to map the clinical features of patients and understand their trajectories. We call this phenotyping. Once we understand the phenotypes we can link this back to the genotype and understand why people with Parkinson&#8217;s disease develop some complications and others do not. We will also be following a group of patients that have increased genetic susceptibility to Parkinson&#8217;s disease, which allows us a key window of opportunity to understand the prodromal/early phase of the disease. The earlier we learn to spot Parkinson&#8217;s disease, the more chance we have of intervening to stop neurons from progressively dying. That’s exciting. 
<h6>What is unique about 23andMe’s data set or our research model that interests you?</h6>
What’s unique is the scale of data that we have and the ability to understand how our genotype influences the risk of developing Parkinson&#8217;s disease and how it may progress. It’s an incredible opportunity to work with a team of scientists so that we can answer important clinical questions and set ourselves up for developing and testing disease-modifying therapies. 
<h6>What are your hopes for the work you are doing?</h6>
My hopes are that we can make a real contribution to understanding not only the risks for developing Parkinson&#8217;s disease by following patients in the prodromal phases but also what’s happening in the lives of patients living with the disease today. I’d hope that this goes back into developing new therapies that target the core of the disease process so that we can prevent Parkinson&#8217;s disease before it emerges or preserve function and stop neurological decline for those already diagnosed.

23andMe Blog

23andMe Blog Team

Introducing the New Lead Scientist for Parkinson’s Research at 23andMe

April is Parkinson’s Awareness Month. It also marks the 12th anniversary of 23andMe’s groundbreaking Parkinson’s Research community, which is now the largest <a href="https://www.23andme.com/research/">genetic research</a> cohort for Parkinson’s disease in the world.
But the power of that research engine wouldn’t be possible without Anne Bossman and thousands of other people like her who have consented to participate in 23andMe research. Anne, a 62-year-old personal trainer living in Colorado, was diagnosed with Parkinson’s two and a half years ago.
<div id="attachment_28836" style="width: 310px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-28836" class="wp-image-28836 size-medium" src="http://35.88.189.111/wp-content/uploads/2021/03/IMG_5405-300x300.jpg" alt="A photo of Anne Bossman near her home in Colorado." width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-1024x1024.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-768x768.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-880x880.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-1180x1180.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405-980x980.jpg 980w, https://blogcms.23andme.com/wp-content/uploads/2021/03/IMG_5405.jpg 1705w" sizes="auto, (max-width: 300px) 100vw, 300px" />Anne Bossman near her home in Colorado. </div>
<h2>Participating in Research</h2>
It hit her hard.
“After my diagnosis, I cried,” she said.
But it wasn’t for long.
“I knew Parkinson’s was not going anywhere, and the sooner I accepted this and plowed forward, the sooner I could have good days,” Anne said.
First, she learned as much as she could about the disease. She used the vast resources of the Michael J. Fox Foundation, and then she was introduced to 23andMe and joined our Parkinson’s Research community.
“I was very happy for the opportunity to participate,” Anne said.
Her participation and the participation of thousands of others in 23andMe’s Parkinson’s Research community have helped fuel insights published in 17 papers, <a href="https://research.23andme.com/publications/#publications">four of them</a> last year alone. That research has always been about using genetic insights to search for better ways to diagnose and treat Parkinson’s disease and possibly make discoveries that could help lead to a cure.
<h2>Staying Active</h2>
For Anne, the most important thing is to stay active.
“(Parkinson’s disease) is known but not understood by almost everybody until it touches their lives directly,” Anne said.
Being active is vital for Anne, and she feels fortunate to have always been an athlete and outdoorsy. Her symptoms include stiffness, but she can overcome some of that by keeping moving, exercising, riding horses, balancing exercise, and lifting weights.
“I feel better the more exercise I get,” Anne said.
She hopes to be able to show others a way through her example.
“It’s not how often I get down,” she said. “But how quickly I can pick myself back up.”
You can learn more about 23andMe’s Parkinson’s Research program <a href="https://www.23andme.com/pd/">here</a> or view another 23andMe Parkinson’s research participant <a href="https://www.youtube.com/watch?v=-1gjNUzABAY">Claudia’s story</a> about participating in the program.

Raising Awareness of Parkinson’s Disease

By Eli Chanoff, 23andMe Research Associate
Parkinson’s disease (PD) has been a central focus of 23andMe’s research since our company’s early years.
Over more than a decade, we have grown a community of tens of thousands of individuals, with and without Parkinson’s, who are committed to making a difference through research. With this community, 23andMe researchers have contributed to more than <a href="https://www.23andme.com/publications/">20 papers</a> offering new insights into the disease. As a result, we are in a unique position to advance our understanding of this disease and, in particular, to investigate genetics&#8217; role in both Parkinson’s disease risk and progression.
<h2>LRRK2 G2019S</h2>
The G2019S variant in the LRRK2 gene is associated with a significantly increased risk of developing Parkinson’s disease. 23andMe launched the Parkinson’s Impact Project (PIP) in 2018 to learn about the experience of people who carry the LRRK2 G2019S variant. The project consists of a comprehensive baseline survey and shorter quarterly follow-up sessions completed by consented research participants who are eligible carriers with and without a diagnosis of PD. The baseline survey was also completed by a large group of consented, eligible research participants without the G2019S variant who were matched to the carriers based on age and sex. 
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-22635" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg" alt="" width="287" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg 287w, https://blogcms.23andme.com/wp-content/uploads/2015/06/Brain-Logo.jpg 438w" sizes="auto, (max-width: 287px) 100vw, 287px" />Less than half of individuals with one copy of the variant develop Parkinson’s disease. Understanding why some carriers develop the disease while others don’t could offer key insights into novel approaches to slowing or stopping disease progression.
In addition, since a higher portion of the carrier population is at risk of being diagnosed with PD, it’s safe to assume that the cohort will also have an increased proportion of individuals with early-stage (prodromal) disease but who have not yet been diagnosed. Therefore, traits enriched in the carrier cohort relative to matched controls may represent early warning signs of Parkinson’s disease. However, these traits could also result from the G2019S mutation entirely unrelated to PD. Follow-up analyses are needed to distinguish between findings due to simply being an LRRK2 G2019S carrier and those due to having early-stage disease.
Although this is very much a work in progress, we strongly believe it is important and appropriate for us to share preliminary data with those participating in the study and the broader community. Below, we review a few of our initial results from the analysis of the baseline survey data.
<h2>Our Findings</h2>
Of those surveyed, 16 percent of G2019S carriers and 2.6 percent of non-carriers reported a diagnosis of Parkinson’s disease. We have separated our cases and controls into those with and without the G2019S variant–regardless of Parkinson’s status–to precisely measure the association between this genetic variant and a set of Parkinson-related phenotypes.
Phenotypes can refer to traits, clinical symptoms, environmental exposures, and comorbidities in this context. When considering the link between any phenotype and Parkinson’s, it is important to remember that a phenotype could be caused by PD, could be a risk factor for PD, or could be an early warning sign of PD. Symptoms are a subset of phenotypes and are distinct from other phenotypes–even physiological ones–because of their use in a clinical setting.
Below is some of the data we gathered from the PIP baseline survey. Please note that presenting with any of these phenotypes does not mean having Parkinson’s disease. Our services are not meant to diagnose or treat any disease. Please contact your doctor or a <a href="https://www.michaeljfox.org/news/movement-disorder-specialists">movement disorder specialist</a> if you want to be evaluated for Parkinson’s.
<h2>Motor Findings</h2>
Motor symptoms, such as tremors, stiff or slow movements, impaired posture or balance, and rigidity, are the characteristics most commonly used to diagnose Parkinson’s disease. While other motor and non-motor phenotypes are also common, these canonical motor symptoms remain more widely studied and are often what first comes to mind when people think about PD.
The baseline survey asked respondents about a series of motor phenotypes derived from the commonly used MDS-UPDRS rating scale, a few of which are included below. This chart shows the percentage of G2019S carriers and non-carriers who reported experiencing trembling or shaking in any part of their body, changes in handwriting, gait, or stooping posture. Recall that both carriers and non-carriers may or may not have a diagnosis of Parkinson’s disease.
These data show that some motor phenotypes previously associated with non-genetic Parkinson’s disease, were reported more frequently by G2019S carriers than non-carriers. While more analysis is needed, early results support the hypothesis that carriers are at increased risk of experiencing these symptoms based on their genetics.
<h2>Non-motor Phenotypes</h2>
In addition to motor symptoms, several non-motor phenotypes have been linked to Parkinson’s disease. However, many of these, such as constipation and cognitive changes, also occur in non-PD populations, and PD also increases in frequency with age, making the selection of appropriate controls very important.
The first chart below shows results from our survey for a few non-motor PD phenotypes. This chart shows the percentage of carriers and non-carriers who reported having trouble concentrating on things, like reading the newspaper or watching television, or who felt down, depressed, or hopeless on at least half of the days in the previous two weeks. It also includes those who reported having fewer than three bowel movements in a typical week.
These data do not clearly show a difference in the risk of developing certain non-motor phenotypes between carriers and non-carriers.
Our survey also asks for additional pieces of participants’ health histories to assess possible links between other health conditions and Parkinson’s disease. Finding an association between PD and another condition may suggest similarities between the biological pathways underlying either disease. Establishing these associations also helps us understand the significance of different PD risk factors.
In this second chart, we show results for a few conditions that are thought to have some relationship with PD. It shows the percentage of carriers and non-carriers diagnosed with or treated for restless leg syndrome, head injury or concussion, and allergies.
Interestingly, these data suggest that having the LRRK2 G2019S variant may increase the risk of having allergies. A previous 23andMe publication titled <a href="https://www.nature.com/articles/s41531-019-0077-5">The Parkinson’s phenome–traits associated with Parkinson’s disease in a broadly phenotyped cohort</a> found a link between seasonal allergies and PD, suggesting a possible similarity in the immune system’s role in both conditions. Our new results support that possibility.
<h2>What’s Next</h2>
The data provided by the respondents to this survey serve as an important first step toward measuring disease progression and potentially identifying clinically useful early signs of PD in LRRK2 G2019S carriers. By participating in our surveys, 23andMe customers fill in the gaps in our knowledge and provide a clearer picture of how this disease manifests.
We are excited to continue this research and are grateful for the many consented research participants who make it possible. As our collection of phenotypic data grows, we aim to share results from the Parkinson’s Impact Project.

Preliminary Results from the Parkinson’s Impact Baseline Survey

A new study that relied on data from more than four million 23andMe customers, may help speed efforts now underway to find drug targets for treating Parkinson&#8217;s disease.
<img loading="lazy" decoding="async" class="alignright wp-image-3133 size-full" src="http://35.88.189.111/wp-content/uploads/2009/03/parkinsonsdisease.jpg" alt="" width="260" height="236" />Working with researchers at 23andMe, scientists at the Broad Institute of MIT and Harvard, were able to identify a very rare group of individuals who have what are called &#8220;loss of function&#8221; alleles in the gene LRRK2. These 1,400 individuals also do not appear any more or less healthy than those without the loss of function alleles, even though the alleles have essentially turned off the function of one of their LRRK2 genes.
This finding, published in the journal <a href="https://www.nature.com/articles/s41591-020-0893-5">Nature Medicine</a>, gives drug hunters looking for new treatments more evidence that they may be able to safely target that gene, which is the most common genetic cause for Parkinson&#8217;s.

<h6>Collaborating and Leveraging Data</h6>
The paper was one of <a href="https://www.broadinstitute.org/node/629796">seven published </a>by the researchers using data from Broad&#8217;s <a href="https://www.nature.com/immersive/d42859-020-00002-x/index.html">Genome Aggregation Database</a> (gnomAD), which brings together exome and sequence data from many sources for researchers. Leveraging that data, the researchers looked not just at Parkinson’s disease, but also developed a catalog of human variation, insights into population genetics, disease association, and diagnostic screening.
A grant from the <a href="https://www.michaeljfox.org/">Michael J. Fox Foundation</a> helped pay for the work on the LRRK2 paper, which included essential contributions from scientists at Imperial College London, and the Icahn School of Medicine at Mount Sinai. The study also included data from the <a href="https://www.ukbiobank.ac.uk/">UK Biobank</a> and Broad&#8217;s gnomAD.
&#8220;The study is another illustration of the immense value of 23andMe&#8217;s data,&#8221; said Paul Cannon Ph.D., 23andMe&#8217;s Parkinson&#8217;s disease research manager. &#8220;Having this very large genetically and phenotypically characterized cohort offers novel opportunities to look for evidence of any potential safety concerns for drugs for targets like these, which individuals at risk of developing Parkinson’s, may end up taking chronically, perhaps for decades .&#8221;
<h6>Looking at LRRK2</h6>
As part of their work, the researchers were also able to confirm many known loss of function variants in the LRRK2 gene, which are extremely rare. But the researchers also found that about 1,400 individuals in the 23andMe database carried one of three loss of function variants. The 23andMe data includes extensive health as well as other <a href="https://www.23andme.com/research/" target="_blank" rel="noopener">phenotypic information</a>. This allowed researchers to determine that those individuals did not appear to be suffering health effects from that loss of function.
In most cases, the cause of Parkinson&#8217;s disease is unknown. There is a complex mix of genetic and environmental factors at play that lead to the development of the disease. But in the last decade, researchers have identified variants in a handful of genes, including <a href="https://ghr.nlm.nih.gov/gene/LRRK2#normalfunction">LRRK2</a>, associated with developing Parkinson&#8217;s disease. In the case of LRRK2 a variant in the gene is associated with the overproduction of certain proteins in the brain. Scientists have long believed that one avenue for treating the disease may lie in modifying, or &#8220;down-regulating&#8221; the function of the LRRK2 gene. Still, they want to better understand whether that can be done safely.
&#8220;These results suggest that drugs that reduce LRRK2 kinase activity are unlikely to show toxicity due to on-target effects,&#8221; the researchers state in the paper.

Large Study Offers Insight into Parkinson’s

Last year marked the tenth anniversary of 23andMe&#8217;s Parkinson&#8217;s Disease Research Community. <img loading="lazy" decoding="async" class="alignright wp-image-22635 size-medium" src="https://blog-api.23andme.com/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg" alt="" width="287" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2015/06/Brain-Logo-287x300.jpg 287w, https://blogcms.23andme.com/wp-content/uploads/2015/06/Brain-Logo.jpg 438w" sizes="auto, (max-width: 287px) 100vw, 287px" />
This community has not only helped our scientists and others make serious advances in the study of Parkinson&#8217;s but it has also ushered in a new approach to genetic research.
As part of Parkinson&#8217;s Awareness Month, we wanted to look back over the now 11 years since we formed the Parkinson&#8217;s Research Community and note some of what we&#8217;ve accomplished.

<h6>Growing Quickly</h6>
Back in 2009, when 23andMe first announced its plan to enroll 10,000 people with Parkinson&#8217;s disease, 23andMe didn&#8217;t even have 10,000 customers. With the help from our collaboration with <a href="https://www.michaeljfox.org/">The Michael J. Fox Foundation</a> (MJFF) and the Parkinson&#8217;s Institute, however, the company met its goal within five years. That milestone was just the first of many, as the community has helped power relevant research and insights into the disease.
Having so many people living with Parkinson&#8217;s participating in our research has meant that 23andMe&#8217;s genetic data repository on Parkinson&#8217;s is materially larger than anything that came before. Now it is by far the world&#8217;s largest cohort of its kind for Parkinson&#8217;s disease research. Now is a great time to reflect on some of our important discoveries and to remember that none of it would have been possible without the active participation of the 23andMe research participants and the dedication of scientists within and outside of 23andMe.
<h6>Some Milestones</h6>
Here are a few highlights:
<ul>
<li>To date, our researchers and collaborators discovered 90 genetic variants associated with the disease. These findings give scientists potential pathways for future research and insight into possible new drug targets to treat Parkinson&#8217;s.</li>
<li>23andMe researchers and collaborators have published 18 papers in peer-reviewed publications, including four in 2020 alone. Among those papers are new findings around <a href="https://www.biorxiv.org/content/10.1101/604033v1">putative causal risk factors</a> for Parkinson&#8217;s, genetic variants that influence the age of onset for Parkinson&#8217;s, and a genome-wide association study that was paired with single-cell gene expression data to help <a href="https://www.biorxiv.org/content/10.1101/528463v2">identify cell types</a> that are important for understanding the causes of Parkinson&#8217;s.</li>
<li>23andMe researchers have identified more than 100 phenotypic — or non-genetic traits or characteristics — associations with Parkinson&#8217;s, offering the potential of earlier detection of the disease.</li>
<li>23andMe researchers, in collaboration with scientists from The Michael J. Fox Foundation, are also pioneering novel ways of collecting and analyzing data to gain deeper insight into the disease. Among these new datasets is one, collected by 23andMe researchers, looking at <a href="https://blog.23andme.com/23andme-research/update-23andme-parkinsons-disease-research/">off-label drug use among Parkinson&#8217;s patients</a>. This is a practice by which doctors use medication approved by the FDA for one condition to treat other conditions for which the medication is not yet approved.</li>
<li>The Michael J. Fox Foundation launched <a href="https://foxinsight.michaeljfox.org/">Fox Insight</a>, an online clinical study to crowdsource data from people with and without Parkinson’s. Through a collaboration with 23andMe, eligible participants can also access the 23andMe Health + Ancestry Service and add their genetic information to the study at no cost. To date, more than 40,000 people are registered in the study — with the goal of recruiting hundreds of thousands more. And more recently, MJFF launched <a href="https://foxden.michaeljfox.org/insight/explore/insight.jsp">Fox DEN,</a> Fox Insight’s online portal to provide qualified Parkinson&#8217;s researchers access to its de-identified data.</li>
<li>We&#8217;ve also recently completed a small-scale pilot study looking at the gut and oral microbiomes of people with Parkinson&#8217;s. We plan to follow this up with a much larger study later this year including healthy controls.</li>
<li>In the past year, 23andMe’s Parkinson’s Disease Research strategy has expanded to include participants who are at increased risk of developing Parkinson’s disease. By participating in this research, people without Parkinson’s disease can help researchers better understand the factors that influence why some people develop Parkinson’s disease. This could help contribute to the development of new interventions and treatments to prevent or slow the progression of the disease. This expansion of research was kicked off with the launch of the Parkinson’s Impact Project, which focuses on individuals that carry the LRRK2 G2019S variant. 23andMe plans to expand research efforts to other at-risk cohorts in the near future.</li>
<li>As part of the Parkinson’s Impact Project, we kicked off enrollment of LRRK2 G2019S carriers, both with and without Parkinson’s disease, into the University of Rochester’s innovative telemedicine study, VALOR-PD.</li>
</ul>
<h6>A Model for 23andMe Research</h6>
<a href="https://www.23andme.com/pd/">23andMe&#8217;s Parkinson&#8217;s Research Community</a> is unique in that it allows for ongoing engagement with participants. In addition, we see that customers are also eager to take an active role. Because these individuals are so engaged, scientists are better able to track changes and understand the progression of Parkinson&#8217;s, as well as nimbly add new dimensions to their research. It may even help in identifying potential participants in clinical studies and accelerate the pace of drug development.
Beyond the participants in the community, 23andMe&#8217;s Parkinson&#8217;s disease research is more potent because of the millions of 23andMe customers who, while not part of the community, opt-in to participate in 23andMe Research. Having such a large number of &#8220;controls&#8221; is vital for researchers.
By leveraging online tools, computational know-how, engaged customers, and massive amounts of both phenotypic and genetic data, 23andMe has pioneered a new way of conducting genetic research over the past ten years. 23andMe&#8217;s ambitious efforts around Parkinson&#8217;s disease, also helped the company create the framework for how it, and now others, approach genetic research into other conditions.
There is no other study cohort with the scale and diversity of 23andMe, which has millions of participants who are both engaged and interested in contributing to research.
<h6></h6>

23andMe’s Parkinson’s Research Community, More than a Decade of Discovery   

We wanted to share this perspective that appeared this week on the Michael J. Fox Foundation <a href="https://www.michaeljfox.org/news/powering-parkinsons-research-my-blueprint">blog</a> from, Claudia Revilla, a long-time 23andMe Parkinson&#8217;s Research participant. Claudia has been inspiring us for years and we want others to hear her voice.
First impressions. For those of us with Parkinson’s disease (PD), we all remember that dreadful day the doctor said:
<div id="attachment_27758" style="width: 292px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-27758" src="https://blog-api.23andme.com/wp-content/uploads/2019/11/Claudia-282x300.jpg" alt="" class="wp-image-27758 size-medium" width="282" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2019/11/Claudia-282x300.jpg 282w, https://blogcms.23andme.com/wp-content/uploads/2019/11/Claudia.jpg 474w" sizes="auto, (max-width: 282px) 100vw, 282px" />Claudia, far right, and her son Carlos, with 23andMe co-founder and CEO Anne Wojcicki. </div>
 &#8220;You have Parkinson&#8217;s.&#8221; 
In my case, almost ten years ago, those words only made sense because I knew that something was wrong — but what followed is what set the direction of my future actions. I carefully listened to every word the doctor was saying and when she asked if I knew of any blood relative with Parkinson&#8217;s, I responded with a “no.” 
Immediately thinking of my children, I asked: 
&#8220;Is Parkinson&#8217;s disease genetic?&#8221; 
<h6>What Can I Do?</h6>
My doctor responded that in most cases, the cause of PD is unknown. We can’t confirm the disease is only genetic. Scientists are working to uncover and understand genetic components and other factors that could lead to Parkinson’s like aging and the environment. 
I went home to my private “library” — the internet — and quickly got involved with <a href="https://www.michaeljfox.org/">The Michael J. Fox Foundation</a>. I was determined to help find a cure. 
As my grandma used to say, “If you want something done right, you have to do it yourself.” 
<h6>Participating in 23andMe Research</h6>
Since I can’t cure this disease all by myself, I joined efforts with those already in the search. Through <a href="https://foxtrialfinder.michaeljfox.org/">Fox Trial Finder</a>, I was matched with many opportunities to participate in PD research. One of them was genetic testing through the personal genetics company <a href="https://www.23andme.com/pd/">23andMe</a>. I immediately remembered the conversation with my doctor — and I signed up right away.
23andMe mailed me a spit kit. I followed the simple instructions — I spat in the tube and sent it back. When I got the results, just a couple of weeks later, I was, and still am in awe. I learned about me. I had information about my genetics that I did not know about. 
I took this opportunity to provide information about my own disease to be part of a larger 23andMe database with other PD patients to help find the many “whys” and “hows” of Parkinson&#8217;s. This is teamwork — through technology — not just to solve problems, but to prevent them from happening.
<h6>The Power of Knowledge</h6>
I never cared much about my own ancestry, but I do care about my health and the health of my future generations. Deciphering the code of what we are made of and how we work is like getting the blueprint of a building — using it to fix whatever breaks down or needs improvement.  
Our blueprint is the human genome, wonderful and unique to each of us. It could lead us to a way to detect, prevent and cure diseases. The power of knowledge about ourselves and our bodies is an inalienable right. It is our choice, whether we use it or not. Scientists researching incurable, progressive and devastating diseases are using genetics to find cures and answers to our ailments.  
<h6>Sharing My Story</h6>
During October, I had the opportunity to participate in a press conference for 23andMe. Myself, along with two other patients, shared our story about getting genetic testing that helped raise flags on important health issues. We all first consulted with our physicians, but the single most important action we took, was getting a 23andMe spit kit. It helped sketch our personal blueprints and empowered us to advocate for our own health.
<h6>My Hope</h6>
I wish there was a test to tell me that I have Parkinson’s. Or, even before I was diagnosed, a gene that would say definitively that I would get the disease. Because I could have taken action much earlier on. But I know these scientific breakthroughs will happen. I am taking action right now to help researchers find clues about Parkinson&#8217;s. 
Researchers have identified a handful of genes, like LRRK2 and GBA, that increase your risk of getting PD. And this has been made possible thanks to the volunteers willing to participate in genetic research. Many more findings will follow with the continued participation of volunteers in genetic research. 23andMe is making this possible and accessible to everyone.  
Back in the Middle Ages, no one dared to sail past the horizon because they believed Earth was flat. It took one brave person to try it — that was a true big step for mankind. Organizations like 23andMe and The Michael J. Fox Foundation are now sailing to the newest horizon. I, too, will follow, until we reach our destination.
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Interested in participating in genetic research? MJFF’s online clinical study Fox Insight is accelerating breakthroughs by capturing the experiences of people with and without Parkinson’s. Through a collaboration with consumer genetics company 23andMe, people with Parkinson’s who join Fox Insight can access the 23andMe Health + Ancestry Service at no cost and add their genetic information to the study. Register at <a href="https://foxinsight.michaeljfox.org/?utm_source=Blog&#038;utm_medium=Website&#038;utm_campaign=MJFF&#038;utm_content=Blog_23andMe_Podcast">foxinsight.org.</a>
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Claudia Garrido-Revilla, member of the Foundation’s Patient Council, has served as a Fox Trial Finder Ambassador and Team Fox member with The Michael J. Fox Foundation. Her advocacy and service activities are not limited to the Parkinson&#8217;s community. She has found that service and advocacy are necessary to keep a community together and healthy, and that volunteers and leaders are needed everywhere and always.

Powering Parkinson’s Research with My Blueprint 

By Tony Garrett, 23andMe customer and research participant
What if something inside you, something in your DNA, could lead to a cure, would you share it? Would you share it even if it didn’t help you personally?<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2019/04/tony3-300x300.jpg" alt="" class="alignright size-medium wp-image-26990" width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2019/04/tony3-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2019/04/tony3-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2019/04/tony3-768x768.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2019/04/tony3-880x880.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2019/04/tony3-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2019/04/tony3-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2019/04/tony3-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2019/04/tony3.jpg 960w" sizes="auto, (max-width: 300px) 100vw, 300px" />
I’m a 40-year-old father of a teenage girl, and this question isn’t a rhetorical one for me. I’ve been<a href="https://www.facebook.com/TGarrettsjourney/?__tn__=kCH-R&#038;eid=ARBqRHv7yt_UH_sT_441d7bX8DDWkPiVBN2x-yOHNwJmA_7E2jOSfQUasc0VDrBS6P1dzg3Tn8aLTTqu&#038;hc_ref=ARTBXtmIVCHjB-3dUkfvP-FK1A_wIz133xA-VzHU_dSc4KPxtvspV15VtSjaOOJX9yk&#038;fref=nf&#038;__xts__[0]=68.ARDjr_zK3QslhTDu2kgxHr4DjjiyjsafrJGjjywzBbXqrz3YRB16qmF_Q-InNzw3uZo6dYM_ISpM5Camrt64jcZ7LcTZ-PUnlgx-oI1z3eEItPSB_4S8aUHRbBStcAnWyJ9IMCicsyOpFXjzweTsbwx75Yquz0WEd3CozZRZMoGYSsutnbHAUwhGe3IzT7UFhnzicn1dQYDlyVCz504j_lNhKwsvQ8uI8hecZMqfOPw6HemaBSB5uehHeUAjF9ulHDD0pX-gDn6WCm_ilyaAPfZjG5Vc1ifKcnF8d4mxu4FurVBuGI3bcXSXmgJKKICaXGRNYLgCw69BG5fl2yyXgQ"> living with Parkinson’s disease</a> for a decade now. I want to know.
I have to tell you I’m biased. I would gladly share my information. I would die happy if I knew that knowledge gleaned from my DNA might have helped in the development of a treatment or cure. Even if it didn’t help me.
<h6>You Can Help</h6>
Something in you, in your DNA, when studied together with data from millions of others, could help me. Isn’t that a profound idea?
What is much more likely is that that information could help future generations facing a diagnosis like mine. That’s why five years ago I didn’t hesitate to opt into having researchers at 23andMe use my data. The company was<a href="https://www.23andme.com/pd/"> upfront</a>. They let me know they were working with researchers at<a href="https://foxinsight.michaeljfox.org/"> The Michael J. Fox Foundation</a> and also at pharmaceutical companies that may use my anonymous data for the study of Parkinson’s and other diseases, in the search for new treatments.
But I know that not everyone is so eager to be part of research like this. I understand that, and I’ve heard a lot from those who choose not to opt-in and all the reasons why. But I want to share with you what I see as the positive side of participating in research.
We live in a new world where data, big data from millions of people like you and me, could lead to new breakthroughs that save people’s lives. This new method of research is revolutionary. It has the potential of accelerating treatments and cures for conditions like Parkinson’s, and to do that much faster than before. For those of us with Parkinson’s that means something.
<h6>Living with PD</h6>
So what about me?
Many people know about Parkinson’s because of Michael J. Fox and Muhammad Ali, and the heroic work they’ve done to raise awareness about this condition. But, like me, most of the almost one million people living with Parkinson’s in the United States are not in the limelight. Our daily battles with this disease are largely unseen.
My life is simple.
<div id="attachment_26991" style="width: 310px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-26991" src="https://blog-api.23andme.com/wp-content/uploads/2019/04/Tony2-300x300.jpg" alt="" class="size-medium wp-image-26991" width="300" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2019/04/Tony2-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2019/04/Tony2-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2019/04/Tony2-768x768.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2019/04/Tony2-880x880.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2019/04/Tony2-271x271.jpg 271w, https://blogcms.23andme.com/wp-content/uploads/2019/04/Tony2-372x372.jpg 372w, https://blogcms.23andme.com/wp-content/uploads/2019/04/Tony2-574x574.jpg 574w, https://blogcms.23andme.com/wp-content/uploads/2019/04/Tony2.jpg 960w" sizes="auto, (max-width: 300px) 100vw, 300px" />Tony with his daughter Breanna.</div>
I was born and raised in a working-class part of Illinois where I still live. I played high school sports — football, basketball, and track. When I graduated, I went to work. I did maintenance with the local school district, but in my early 20s I noticed my hand was giving me trouble, and my pinky would shake. My doctor sent me to see a neurologist, but at the clinic, they told me they’d need me there for two weeks of tests. I couldn’t take that kind of time off work. It would be several years before I was ultimately diagnosed, at 31, with young onset Parkinson’s disease.
By then I was having more than just grip problems. I had leg cramps, slurred speech, and some mornings it was so hard to move. It felt as if I was encased in concrete. My doctor said I was the youngest patient he’d ever seen with the disease. I guess that makes me special.
<h6>What I Want</h6>
I tell you this not so that you will feel sorry for me. I don’t want pity. I want you to understand what it is like to live with a condition like Parkinson’s. It’s a daily struggle. It involves both physical and psychological pain, wrangling for the right treatment, finding a medicine that doesn’t cause you even more problems, and fighting off depression. And as with any incurable condition, you must come to terms with where this is all going. Where it ends.
But I’m OK. My diagnosis brought me closer to my God. It has distilled what is essential in my life — my daughter, and my family. It helped me focus on the joy, and satisfaction I get in helping others. And I’ve learned to appreciate the simple joys of a walk outside and the morning sun. But I wouldn’t wish this disease on anyone. I will do whatever I can to help find a cure.
This gets me to you, and the question I asked in the beginning:
What would you do if information inside your DNA, could help cure Parkinson’s or any number of other conditions? Would you share it?
Tony Garrett is a retired maintenance worker who now works to raise awareness about Parkinson’s disease. He lives in Evanston, Illinois.
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Participating in 23andMe Research, A Customer’s Perspective

New Parkinson&#8217;s disease research by scientists at 23andMe has identified more than 100 phenotypic variables related to the disease, offering a potential step forward in efforts to diagnose Parkinson&#8217;s disease earlier.
<div id="attachment_24396" style="width: 260px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-24396" src="https://blog-api.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-199x300.jpg" alt="" class="wp-image-24396" width="250" height="376" srcset="https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-199x300.jpg 199w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-768x1156.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-680x1024.jpg 680w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-585x880.jpg 585w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-784x1180.jpg 784w, https://blogcms.23andme.com/wp-content/uploads/2016/10/KarlHeilbron-preferred-scaled.jpg 1701w" sizes="auto, (max-width: 250px) 100vw, 250px" />Karl Heilbron, Ph.D.</div>
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Published today in the <a href="https://www.nature.com/npjparkd/">Nature Partners Journal/Parkinson’s Disease</a>, the new <a href="https://www.nature.com/articles/s41531-019-0077-5">paper</a> offers a wider glimpse of the phenotypes — traits, environmental exposures, and comorbidities — that are linked to Parkinson’s disease, such as migraines, obsessive-compulsive disorder, and seasonal allergies. This study was a collaborative effort with Alastair Noyce from the Preventive Neurology Unit, Queen Mary University of London and Mike Nalls from the National Institute on Aging and Data Tecnica International.
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“Understanding which conditions are associated with Parkinson disease — particularly those that often occur much earlier than the typical age of diagnosis — is a promising step forward for the Parkinson’s community,&#8221; said <a href="https://blog.23andme.com/23andme-research/update-23andme-parkinsons-disease-research/">Karl Heilbron</a>, Scientist I, Statistical Genetics, 23andMe. “Especially in terms of being able to identify those that might develop Parkinson’s much earlier, it’s possible to envision a future where we could intervene before the condition develops in the first place.”
<h6>Research Platform</h6>
This study is part of a broader effort by 23andMe over the last decade to use genetics to advance our collective <a href="https://blog.23andme.com/news/on-our-way-to-10000-23andme-welcomes-first-members-of-parkinsons-disease-community/">understanding of Parkinson’s Disease</a>. That effort has benefited from a long-standing collaboration with The Michael J. Fox Foundation (MJFF), most recently with the <a href="https://blog.23andme.com/research-communities/october-insights-into-parkinsons-research/">Fox Insight study</a>.
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“These novel associations provide insights into potential causes and contributing factors of Parkinson’s,” explains <a href="https://www.michaeljfox.org/foundation/leaders.html?subcatid=381">Brian Fiske</a>, PhD, Senior Vice President, Research Programs at MJFF. “This information may ultimately help researchers develop new diagnostic tools and treatments.”
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For this latest study, 23andMe researchers were able to leverage our unique research platform. The platform includes both phenotypic and genetic data from millions of customers — some with Parkinson’s and others without it — who have consented to participate in research.  
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<h6>Parkson&#8217;s Associations </h6>
The researchers included data from 13,196 people with Parkinson’s disease as well as data from 131,960 other individuals who do not have the disease. The study revealed that having Parkinson’s disease was associated with 122 phenotypes, 27 of those were previously known to be associated with the disease, and another 23 had a strong a priori link to a known association. 
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But importantly, the researchers discovered 42 associations that have not previously been reported. Furthermore, researchers found that migraines, obsessive-compulsive disorder, and seasonal allergies were associated with Parkinson’s disease. And these phenotypes tended to  occur decades before the typical age of diagnosis for Parkinson’s disease. 
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By better understanding what traits are “flags” for the disease, it may help lead to earlier diagnosis and eventually screening. While this doesn’t mean that just because you have migraines or seasonal allergies, you’ll develop PD. However, it does have the potential to improve risk prediction, as many currently available algorithms simply don’t have enough information. 
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To date, no disease-modifying drug trial for PD has succeeded. This may be because by the time an individual is diagnosed, they have already lost 30-50 percent of the neurons in the substantia nigra (the brain region linked to Parkinson’s disease motor symptoms), and it may be too late to intervene.
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<h6>Hope for Parkinson&#8217;s Disease Early Detection</h6>
But, with a better understanding of earlier disease associations, perhaps we could develop treatments that can help earlier on.
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“The results of this study could prove to be very valuable. The 23andMe data provide us with a unique opportunity to undertake a comprehensive survey of things that might be important to Parkinson’s disease and, in doing so, we find new associations and confirm the importance of previously recognised associations”, said Alastair Noyce, PhD, Clinical Senior Lecturer in the Preventive Neurology Unit at the Wolfson Institute of Preventive Medicine, Queen Mary University of London. “Some of these are features of established disease, but others occur much earlier in life and may prove crucial to the efforts aimed at defining groups at-risk of Parkinson’s disease, who may be eligible for neuroprotective drugs as these become available.”
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The phenotypes that currently comprise the Parkinson’s disease phenome have mostly been explored in relatively small purpose-built studies. Using a single large dataset, the research team has successfully reproduced many of these established associations and have extended the Parkinson’s disease phenome by discovering novel associations. 
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This work paves the way for studies of these associated phenotypes that explore shared molecular mechanisms with Parkinson’s disease, infer causal relationships, and improve our ability to identify individuals at high-risk of Parkinson’s disease.
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New Parkinson’s Disease Research May Offer Promise for Early Detection

23andMe’s commitment to Parkinson’s research is in the company’s DNA. It goes back almost a decade to when we first launched our<a href="https://www.23andme.com/pd/"> Parkinson’s research community</a>, and  for many of us this interest is more than just professional, it’s personal.
<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2018/10/Run-DNA-Fox-Trot-300x225.jpg" alt="" class="alignright size-medium wp-image-26638" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2018/10/Run-DNA-Fox-Trot-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2018/10/Run-DNA-Fox-Trot-768x576.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2018/10/Run-DNA-Fox-Trot-1024x768.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2018/10/Run-DNA-Fox-Trot-880x660.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2018/10/Run-DNA-Fox-Trot-1180x885.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2018/10/Run-DNA-Fox-Trot.jpg 2048w" sizes="auto, (max-width: 300px) 100vw, 300px" />
We have both friends and family members who are living with the disease. Last month our Parkinson’s research community manager, Paul Cannon,<a href="https://blog.23andme.com/research-communities/an-interview-with-23andmes-parkinsons-disease-program-manager-paul-cannon/"> shared his experience</a> of undergoing surgery for Deep Brain Stimulation for treatment of his Parkinson’s.
 Paul’s experience and others is what helps motivate the work and efforts like 23andMe’s recent sponsorship of fundraisers like the The Michael J. Fox Foundation’s (MJFF) Bay Area Fox Trot 5k to raise money and awareness for Parkinson&#8217;s research. This year our team — 23andMe Run DNA — of more than 100 employees and their family members raised about $12,000. 

This fun way of getting involved also highlights one of our strongest allies in our efforts in Parkinson’s disease, MJFF. One year ago, the Foundation launched a new Parkinson’s research initiative called<a href="http://foxinsight.org"> Fox Insight</a> in collaboration with 23andMe.
Fox Insight is an online clinical study that collects self-reported data about health experiences from those with and without Parkinson&#8217;s, and aims to transform the search for better treatments for the disease. 23andMe and The Michael J. Fox Foundation have joined forces to help eligible participants add their genetic data to this study, which can allow researchers to create a more holistic understanding of the disease. This folds neatly into 23andMe’s long-standing goals of better understanding, treating and preventing the disease.

In the last year, Fox Insight enrollment has more than quadrupled to over 27,000 people and counting, and we hope that thousands, even hundreds of thousands, more will participate.
To educate people about genetic research and how it could help us overcome knowledge and treatment gaps in Parkinson&#8217;s, MJFF created a new video to explain what genetics is teaching us about the disease. As movement disorder specialist and Michael J. Fox Foundation Scientific Advisor Dr. Susan Bressman puts it,
“Advances coming out of genetic research today offer one of our best chances to develop drugs that will help everyone living with Parkinson’s whether they have a (genetic) mutation (for the disease) or not.”
That’s because insights from genetic research can help scientists better understand how Parkinson’s develops, why it manifests itself differently in some people, and why some individuals who carry a genetic mutation associated with Parkinson’s never develop the disease. Studying both those with and without Parkinson’s illuminates these questions. Take a moment to check out the <a href="https://youtu.be/SwQojrAZV9M">video</a> and learn more about<a href="http://foxinsight.org"> Fox Insight</a>.

Parkinson's Disease — Page 2