<img loading="lazy" decoding="async" class="alignright wp-image-4013 size-full" title="geneticresearch7" src="http://35.88.189.111/wp-content/uploads/2009/07/geneticresearch7.jpg" alt="" width="350" height="268" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/07/geneticresearch7.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/07/geneticresearch7-300x230.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Recently, Todd Sherer, CEO of The Michael J. Fox Foundation (MJFF), Brian Fiske, vice president of research programs at MJFF, and Emily Drabant, 23andMe’s research manager for its <a href="https://www.23andme.com/pd/" target="_blank" rel="noopener noreferrer">Parkinson’s community,</a> sat down and took stock of the recent advances in Parkinson’s research.
Their conversation centered around new understandings of the genetics of Parkinson’s disease that could form the building blocks for research over the next decade.
Learning more about the role genetics plays in Parkinson’s could provide life changing new treatments for people living with the disease. &nbsp;Much of the work to this end is currently focused on a particular mutation in the LRRK2 gene. About one in 10,000 people have this particular mutation – G2019S – which is associated with a 50 percent lifetime risk of Parkinson’s compared to about one percent in the general population. While this association is well established, the role the mutation plays in the development of the disease is less clear. Researchers, however, have made some important breakthroughs offering insight into the possible role that LRRK2 plays in developing the disease, as well as how genetics may interact with environmental factors to cause Parkinson’s.
<h6>LRRK2 and Neuroinflammation</h6>
Fiske said new data suggests the body’s immune system, particularly the<a href="https://www.ncbi.nlm.nih.gov/pubmed/21552986"> inflammatory response in the brain</a>, may play a key role in the development of Parkinson’s. Inflammation is the body’s response to injury, but the response, particularly an exaggerated immune response, could lead to harmful neuroinflammation. It appears that one component of Parkinson’s is this harmful neuroinflammatory response. 
Researchers, supported by MJFF, are studying whether the LRRK2 mutation leads to a more exaggerated inflammatory response. &nbsp;To date, the data are looking very interesting in this direction.
<img loading="lazy" decoding="async" class="alignright wp-image-12055 size-medium" title="DSC_5239_Todd Sherer, PhD" src="http://35.88.189.111/wp-content/uploads/2012/04/DSC_5239_Todd-Sherer-PhD-201x300.jpg" alt="" width="201" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/04/DSC_5239_Todd-Sherer-PhD-201x300.jpg 201w, https://blogcms.23andme.com/wp-content/uploads/2012/04/DSC_5239_Todd-Sherer-PhD-768x1147.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/04/DSC_5239_Todd-Sherer-PhD-589x880.jpg 589w, https://blogcms.23andme.com/wp-content/uploads/2012/04/DSC_5239_Todd-Sherer-PhD-790x1180.jpg 790w, https://blogcms.23andme.com/wp-content/uploads/2012/04/DSC_5239_Todd-Sherer-PhD-686x1024.jpg 686w, https://blogcms.23andme.com/wp-content/uploads/2012/04/DSC_5239_Todd-Sherer-PhD-scaled.jpg 1715w" sizes="auto, (max-width: 201px) 100vw, 201px" />Todd Sherer, PhD
Sherer said that one high level theory is that if this connection is real this could explain why not everyone with the LRRK2 mutation develops Parkinson’s.
“To activate the immune system response you need some kind of trigger,” he said. “It may take a trigger to interact with the genetics, but no one has tested for this yet.”
<h6>LRRK2 And Cellular Pathways</h6>
Just as in everyday life we accumulate clutter and waste that eventually has to be thrown out, inside our bodies our daily functions produces trash of sorts that has to be cleared out. Our cells actually have a sort of self-cleaning mechanism called “autophagy” that clears out junk protein and other cellular debris.
Parkinson’s researchers have found that this process is somehow broken in patients with the LRRK2 mutation. Studies are focused on whether decreased autophagy may make cells in the brain more susceptible to Parkinson’s-related cell death. Researchers want to know if this is a cause for the disease or simply an effect from it, said Fiske.
<img loading="lazy" decoding="async" class="alignright wp-image-12056 size-medium" title="Brianfiske" src="http://35.88.189.111/wp-content/uploads/2012/04/Brianfiske-300x200.jpg" alt="" width="300" height="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/04/Brianfiske-300x200.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Brianfiske-880x586.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Brianfiske-768x511.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Brianfiske-1024x681.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Brianfiske-1180x785.jpg 1180w" sizes="auto, (max-width: 300px) 100vw, 300px" />Brian Fiske, PhD
<h6>LRRK2 Clinical Observations</h6>
Researchers are comparing individuals who have the LRRK2 mutation and Parkinson’s with people who have developed the disease but don’t have the LRRK2 mutation. These patients who have the disease but don’t have the mutation are also known as “idiopathic” Parkinson’s patients. Researchers found that while the disease in these two types patients appears to be very similar, in some cases the LRRK2 patients have somewhat milder symptoms. For instance, the loss of smell is less pronounced in LRRK2 patients.
According to Fiske work comparing these patients has also highlighted some other intriguing links that researchers would like to explore.. For example, there is an apparent link between LRRK2 and an increased risk for non-skin cancers. This may have to do with a shared genetic background among people of similar ancestry, for instance, instead of some other causal link, but The Michael J. Fox Foundation’s LRRK2 Cohort Consortium is looking into this connection.
<h6>Other Genetic Factors for Parkinson’s</h6>
When exploring the genetics underlying the disease, researchers are still trying to understand why the LRRK2 mutation sometimes doesn’t lead to development of the disease. Scientists also want to know why the age at which a person develops Parkinson’s is so variable, said Sherer. What is clear is that there are other genetic and environmental factors involved.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-12100" title="emily" src="https://blog-api.23andme.com/wp-content/uploads/2012/04/emily-240x300.jpg" alt="" width="240" height="300">Emily Drabant, PhD
And while there is a lot of focus on the LRRK2 mutation, other genetic factors are also involved. Last year 23andMe found<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002141"> two new genetic associations</a> with the disease and more recently found a genetic variant,<a href="https://www.23andme.com/about/press/sgk1/"> SGK1,</a> that is potentially protective against the disease. Other genetic mutations associated with the disease include one protein primarily found in brain tissue called alpha-synuclein, which is encoded by the SNCA gene. Researchers have found that alpha-synuclein accumulates and clumps together in the brain of Parkinson’s patients. There currently is a clinical trial for a drug that specifically targets these clumps of alpha-synuclein as a way to treat Parkinson’s patients.
There are other genetic variants that are also being looked at, and there is a much broader effort to do a sort of “mega” meta-analysis that would develop a master list of common genetic variants associated with the disease. It’s believed that together these genetic variants account for about a quarter of all Parkinson’s cases, but most of those genetic associations have yet to be discovered. 23andMe and MJFF &nbsp;are part of this large-scale effort. Some of this work may be helped as the cost of exome sequencing and full genome sequencing continues to drop. Most recently an association with a variant in the VPS35 gene was found through exome sequencing. 
“It’s one of the first PD genes found (through exome sequencing) so it represents a technological turning point away from the classic (genome-wide association study) approaches in the past,” said Fiske. “It seems to play roles in pathways involved in transport of proteins around the cell, but we have little understanding yet of how it might lead to Parkinson’s.”
<h6>Parkinson’s Indicators</h6>
Another thrust of the research is into biomarkers that can be used to track the progression of Parkinson’s and may help in early intervention. It could be that looking at alpha-synuclein or another protein called DJ-1 may offer a good way to track the disease. In the case of alpha-synuclein, it might be that detecting clumps of the protein could offer a good measure. There is also the possibility of piggybacking on a technique developed for brain imaging of Alzheimer’s disease. That method, looking at the beta-amyloid protein, could be copied in some way with Parkinson’s patients. 
Researchers are now able to use a brain scan, called the DATSCAN, to measure dopamine in the brain. But while the scan is good for detecting deficits in people in early stages of the disease, those deficits don’t change significantly after a patient has full-blown Parkinson’s, said Fiske. New imaging technologies could be used not just to diagnose the disease and its progression, but also to test the effectiveness of drug treatment.
Finally, while there is a lot of attention focused on treatment, there is also work being done to try to detect Parkinson’s earlier and earlier. Researchers already know that people in Parkinson’s earliest, or “pre-motor” phase, have distinct symptoms, such as loss of smell, sleep problems and constipation. In combination, those symptoms can be a good predictors of Parkinson’s. By identifying those with high risk of developing the disease, it may be easier to target them with new drugs or other therapies to prevent them from ever developing Parkinson’s.
<h6>Conclusion</h6>
New understandings of the genetics of PD offers much to be hopeful about. Parkinson’s is an extremely complex disease, but researchers are finding more and more pieces in our effort to complete our understanding of this sometimes puzzling disease. We are lucky to have so many resources to help us do that. This update really only scratches the surface of the work being done to find treatment and a cure for Parkinson’s. We hope to follow up with another update on the promising Parkinson’s research later this year.

23andMe Blog

23andMe Blog Team

The State of the Science of Parkinson’s Research

<img loading="lazy" decoding="async" class="alignright wp-image-12123 size-full" title="sweets" src="http://35.88.189.111/wp-content/uploads/2012/04/q2.gif" alt="" width="194" height="147" />
As part of<a href="http://www.parkinson.org/"> Parkinson’s Awareness Month</a> 23andMe is releasing <a href="https://www.23andme.com/about/factoid/pd_phewas_personality" target="_blank" rel="noopener">the first</a> of three surprising associations we’ve found between Parkinson’s and certain traits.
The associations are surprising because they appear so unrelated to the disease itself, but they may offer insight into the direction for future research.
Parkinson’s is a degenerative brain disorder, but sifting through the data 23andMe scientists have found associations with such things as personality types, joint pain and levels of cholesterol.
These associations may indicate true relationships between say, cholesterol metabolism and the development of Parkinson’s, or they may simply reflect some other underlying phenomenon.
We don’t know yet, but we do know that other similar odd associations – such as some Parkinson’s patients developing a “sweet tooth,” or losing their sense of smell – have helped researchers diagnose and track the progress of the disease, which initially can be difficult. For instance, the loss of smell is associated with the loss of dopamine receptors in the brain, and it is an early indicator of the disease. The sooner Parkinson’s can be diagnosed the sooner treatment can start.
23andMe researchers looked at more than 1,000 different traits, conditions and diseases to find these associations with Parkinson&#8217;s. At the very least, they open up interesting directions for further inquiry.

Unexpected Associations with Parkinson’s

Recently, we invited a local support group for men with early onset Parkinson’s to come to our office. The idea was to give these guys a chance to learn about about 23andMe and our Parkinson’s Research Community, but we probably learned as much if not more from them then they did from us.
23andMe’s Parkinson’s Research Community has already made great strides and discovered new insight into the disease. In a short time we’ve grown to include more than 7,300 participants. But we are still short of our goal of gathering together 10,000 people with Parkinson’s to join in our effort to beat the illness.
Over beer and pizza, the men talked about how surprising it was that, given the numbers of people with Parkinson’s, more haven’t joined 23andMe’s Research Community. But the group also acknowledged a common refrain for those dealing with a diagnosis – it is sometimes easy to go into denial about it.
Indeed looking around at the men in the room you wouldn&#8217;t know that any were suffering from a degenerative disease. Most of them are still in the prime of their lives, with thriving careers and active families. But it is this ability to maintain appearances that allows some with Parkinson’s to wait to tackle issues with their illness. It may also be why participation in Parkinson’s research as a whole is lower than for many other diseases.
It is here that the men said 23andMe could help the most by engaging and involving patients in research. During what turned into a great brainstorm session the men offered many ideas for ways that we could reach our goals and serve the research community.
We hope to continue these types of events for all of our research communities. If you have ideas or suggestions, please feel free to share them with us in the comments below.
If you or someone you know has been diagnosed with Parkinson&#8217;s disease, please learn more at <a href="https://www.23andme.com/pd">www.23andme.com/pd</a>.

Beer, Pizza and Parkinson’s: 23andMe Hosts Parkinson’s Support Group

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During Parkinson’s Awareness Month, we’ll be highlighting promising research and new findings in the fight against Parkinson’s.
Along the way we hope to boost enrollment in 23andMe’s <a href="https://www.23andme.com/pd/">Parkinson’s Research Community</a> past 7,500 people, getting us that much closer to our ultimate goal of 10,000 people in the community. Enroll and you’ll be in good company &#8212; boxing legend Muhammad Ali, who has Parkinson’s, <a href="https://www.23andme.com/about/press/pdandali/">recently joined</a> 23andMe’s fight against the disease.
In the coming weeks we’ll be writing about the state of the science in Parkinson’s research, we’ll roll out surprising associations between the disease and certain traits, as well as hear from fascinating people living with the disease. All this is not just to draw attention to genetic research, but also to remind people what it means to live with Parkinson’s.
Each year there are more than 50,000 cases of Parkinson’s diagnosed, adding to the more than one million people living with the disease in the United States. Worldwide there are an estimated four to six million people with Parkinson’s, but taking action now to find a cause and cure for the disease could help not just those with the disease but people who may develop Parkinson’s in the future.
<div style="float: right; text-align: justified; width: 200px; background-color: #eee; padding: 15px; margin-left: 10px;">Don&#8217;t Have Parkinson&#8217;s? 
Even if you don’t have Parkinson’s you can help simply by becoming a customer at 23andMe who consents to research and completes surveys. It’s as easy as that. Recently our scientists found a genetic variant that appears to be protective against Parkinson’s, a discovery that wouldn’t have been possible without participation from people who don’t have the disease. Plus, you can learn about your own health and ancestry through the 23andMe Personal Genome Service ®.</div>
Together with our Parkinson’s Research Community, and our partners like<a href="http://www.michaeljfox.org/"> The Michael J. Fox Foundation</a>,<a href="http://www.thepi.org/"> The Parkinson’s Institute</a> and<a href="http://www.parkinson.org/"> The National Parkinson Foundation</a>, 23andMe has already made some promising findings. We’ve discovered <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002141">new genetic associations</a>, replicated 20 other known associations and found a genetic variant that<a href="https://www.23andme.com/about/press/sgk1/"> may be protective</a> against the disease – all that in just a year’s time. This is just the beginning.
As Senator Debbie Stabenow, the co-chair of the Congressional Caucus on Parkinson&#8217;s Disease, said when the Senate <a href="http://www.gpo.gov/fdsys/pkg/CREC-2012-03-29/html/CREC-2012-03-29-pt1-PgS2259.htm" target="_blank" rel="noopener noreferrer">passed a resolution</a> making April &#8220;Parkinson&#8217;s Awareness Month,&#8221; the focus in the coming weeks is meant to &#8220;honor those who live with Parkinson&#8217;s and encourage those conducting the medical research that could hold the key to new breakthrough treatments.&#8221;
You can help. If you have Parkinson’s disease please <a href="https://www.23andme.com/pd">join the 23andMe Parkinson’s Research Community</a> and participate in research that will help speed discoveries. If you know someone with Parkinson’s, let him or her know what we’re doing. Participation is free and you could play a role in making breakthroughs that help you and others with Parkinson’s. There’s also the fun of being part of the broader 23andMe Community, where you can explore your genetics and ancestry.

Parkinson’s Awareness Month 2012

At a Las Vegas gala celebrating Muhammad Ali’s 70th birthday, we premiÃ¨red the video <a href="https://www.23andme.com/pd/" target="_blank" rel="noopener noreferrer">&#8220;Give Us Your Hand,&#8221;</a> featuring the boxing legend and his involvement with 23andMe’s Parkinson’s Disease Research Initiative.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-11314" title="muhammadhomepagegrab" src="https://blog-api.23andme.com/wp-content/uploads/2012/02/muhammadhomepagegrab-300x184.jpg" alt="" width="300" height="184" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/02/muhammadhomepagegrab-300x184.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/02/muhammadhomepagegrab-768x471.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/02/muhammadhomepagegrab-880x540.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2012/02/muhammadhomepagegrab.jpg 981w" sizes="auto, (max-width: 300px) 100vw, 300px" />
By Emily Drabant
As the Research Manager for the <a href="https://www.23andme.com/pd/" target="_blank" rel="noopener noreferrer">23andMe Parkinson’s Community</a>, I spend my days thinking about ways to advance this research faster, cheaper and more effectively than ever before. We launched this project in 2009 and since that time have been going full steam to make this the largest and most scientifically productive Parkinson’s research cohort in the world. We’ve succeeded on the first goal and already have the world’s largest group of people with Parkinson’s participating in genetics research. And we are making strides towards the second goal with <a href="https://www.23andme.com/about/press/sgk1/" target="_blank" rel="noopener noreferrer">significant scientific discoveries last year</a>.
While our progress is incredible, we have not yet reached our primary milestone of enrolling 10,000 people with Parkinson’s. Our team of scientists believes that having a group of that size will put us in a new era of Parkinson’s research. This will dramatically increase the odds of really understanding the genetics behind the disease. Scientists call this the “statistical power” of research. We call it the power of our research revolution.
<div style="float: right; text-align: justified; width: 300px; background-color: #eee; padding: 15px; margin-left: 10px;">
Meeting ‘The Greatest’ 
By Melissa del Sol
“Let me tell him that you’re ready for him. He just finished eating his chocolate doughnut in the other room.”
Yes. Those were the first words the wife of “The Greatest” used to refer to Muhammad Ali, and they were the perfect first words for her to say. At that point, I was thinking, “Muhammad Ali eats chocolate doughnuts? Yes, he is human! Hmmm&#8230; a chocolate doughnut sounds really good right about now&#8230;”
But I digress.
Rewind to the night before, when Emily, our Parkinson’s Disease Research Manager, and I landed at an airport near Ali’s home. Emily and I had no idea what to expect, but we knew we were excited. One of the world’s most recognized sports figures was about to join our fight against Parkinson’s, and we were about to watch it unfold.
The next morning, five dress changes and two IHOP breakfasts later, we started our drive to Ali’s home. Lonnie, his wife, graciously welcomed us in with an open mind and nothing short of an open heart. We immediately started setting the stage for the magic that was about to happen. It was a perfect morning; the light shone in at just the right angles, the air was filled with hope, and the ease of the set up was quite calming.
And then he appeared&#8230;Muhammad Ali came gliding in using the Ferrari of walkers, with the grace of a well-known fighter and the aura of a legend. Not normally star-struck, I didn’t know what to do. I wanted to shake his hand, give him a hug, and let him know how honored we were to have him on our team, but I could barely get out a “hello.” And just like that, he sat down in the beautiful lighting, and we started to film. I remember that first moment his hand appeared on the film monitor; it was so beautiful, I couldn’t help but start to get a little emotional in that quiet space. I knew our film would focus on his hands, but I really did not anticipate seeing the extent of the power that hands have, to draw you in and share with you a reflection of a life journey.
After filming his hands, we moved on to filming his face and some action shots with Lonnie. Muhammad was quiet, but it was clear that inside he has a vivacious, soulful spirit. Muhammad came to life and even smiled a bit, as his wife shared comical college stories. The charisma in his eyes was just like what I saw in every video and documentary I viewed in preparation of our visit.
What happened in those seven hours, I still can’t eloquently explain, but my hope is that our video will reflect a glimpse of our experiences that day.
As we reached the gates to leave his community, that’s when I lost my composure. I started to cry, not because I was sad or because I felt hopeless, but because I had realized that my experience with the Alis had really hit close to home. Muhammad and Lonnie are a replica of a couple that is very close to my heart. Lonnie cares for Muhammad with every inch of her mind and body. She stands boldly and never allows sadness into her home. Just like the other couple I know, after decades of marriage, they still laugh at each others’ jokes, exchange loving glances, and compassionately hold hands. And just like Muhammad, the man in that other couple has Parkinson’s Disease. Similarly, his eyes are full of life. And just like Muhammad showers his children and grandchildren with love, the love that the man I know has for me, is unparalleled.
My visit with the Alis was not about meeting “The Greatest” or a three-time heavy-weight champion, or any other well-deserved title he has earned throughout the years. It was about meeting a husband, a father, and a grandfather, who just like millions of Americans, looks Parkinson’s in the eye and says, “this is but another fight.” I am so proud to be a part of something so special. I truly believe that there will be “power in numbers” with this fight, and I know that 23andMe’s research will empower those who currently face Parkinson’s Disease and forever have an impact on the disease.
As I came back to the office that Monday morning, everyone wanted to know, “What was he like?,” “What did he say?,” “How did it go?” I couldn’t truly explain the magic that Muhammad, Lonnie, Emily, Elliott (our producer), Rick (our videographer), and I had experienced, as it was a moment in time, a memory that could not be re-created. But at the core, it was simple: Muhammad Ali is a gracious man, a human being just like you and me, who happens to be a man of great vision, a man who has changed lives, and a man who will continue to change lives for years to come.
</div>
As enrollment slowed around 6,000 people, I began to brainstorm on ways to get more people with Parkinson’s involved. We’ve worked directly with many patient advocacy groups to spread the word – especially with the <a href="http://www.michaeljfox.org/" target="_blank" rel="noopener noreferrer">Michael J. Fox Foundation</a>, the <a href="http://www.parkinson.org/" target="_blank" rel="noopener noreferrer">National Parkinson Foundation</a>, and <a href="http://www.thepi.org/" target="_blank" rel="noopener noreferrer">The Parkinson’s Institute</a>. But I wondered: how could we reach people who aren’t linked up with an advocacy group or a support group, and perhaps aren’t even very public about the fact that they have Parkinson’s? I began to think that if we did something really big – if we made a splash in a really public way – that it would truly raise awareness about this research and give people who want to participate the chance to do so. I hear from people with Parkinson’s all the time saying ‘I had no idea this was available. I didn’t know I could advance research from home”.
In considering ways to make this research public in a really big way, we naturally started to think about working with a celebrity with Parkinson’s. At the top of that list is Muhammad Ali, one of the world’s most recognized athletes, who has been fighting Parkinson’s for 25 years. We spoke to one of our collaborators, Dr. Bill Langston, and he suggested we contact Muhammad’s wife, Lonnie. “When Lonnie says something is going to happen, she will make it happen,” he said.
Those words were completely true. In December, my colleague, Melissa Del Sol, and I flew to Arizona to film Muhammad and interview Lonnie at their home. It was a magical experience and you can read more in Melissa’s blog.
I didn’t plan to conduct the interview – the director of the video was going to handle that – but at the last minute he decided it made more sense for me to do it. I did it off the cuff and asked questions that I wanted to know as a scientist, as someone with personal connections to Parkinson’s, and as an admirer of Muhammad Ali.
We talked about Muhammad’s diagnosis of Parkinson’s. When he first started showing symptoms they were quite minor – a tremor in his finger. The doctor said it was Parkinson’s syndrome, which meant that it would never progress into full blown Parkinson’s, but rather was just a Parkinson’s-like symptom. But over time his symptoms did progress. When they went to a Parkinson’s specialist he confirmed that it was in fact Parkinson’s disease. I asked Lonnie how they both reacted to this.
“Muhammad deals with adversity a lot different than most people. To him, I don’t think it really registered, because he was still doing a lot of what he wanted to do,” she said. “He’s always had that thing about mind over matter … where he thought he could overcome this on his own. It took a real long time for him to realize that it wasn’t going to work that way.”
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-11327" title="Emily&amp;Melissa" src="https://blog-api.23andme.com/wp-content/uploads/2012/02/EmilyMelissa-300x257.jpg" alt="" width="300" height="257" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/02/EmilyMelissa-300x257.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/02/EmilyMelissa-768x659.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/02/EmilyMelissa-1024x878.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2012/02/EmilyMelissa-880x755.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2012/02/EmilyMelissa-1180x1012.jpg 1180w" sizes="auto, (max-width: 300px) 100vw, 300px" />
“However for me it was a little bit different because when you say disease it is a lot different than hearing syndrome. Any “disease” sounds very fatalistic. So I had to do a bit of investigating.”
As Lonnie learned more, she and Muhammad started to get involved in research. When he realized that he could advocate for others with Parkinson’s, he decided to go public with his diagnosis. Muhammad and Lonnie founded the Muhammad Ali Parkinson’s Center in Arizona in 1997 and have made tremendous contributions to research.
“Muhammad and I have sort of grown up with the research,” Lonnie said. “A lot of research has been done to advance our understanding of what this disease is and where it comes from and some of the factors that may contribute to it. So we are very hopeful about the research. But when we first started out it was funny because we were told that in ten years we would have a cure and it’s just a function of money. Well now we know that’s not true. Ten years have come and gone and there has been a lot of money, but it’s a lot more complex than that. … We are really hopeful that this is one of the neurological diseases that will be given a cure.”
This point is not lost on us at 23andMe. Indeed, the slow pace of research into Parkinson’s and many other diseases was what motivated us to launch our online research platform for all in the first place. We wanted to speed up research and do it bigger than ever before. We knew we needed to change the research model if we were going to make progress in the same lifetime as those who are currently battling Parkinson’s.
“I think 23andMe is cutting edge technology that has been introduced to address this illness and to look at it in a different lens; getting to the genetic basis of what causes this illness, why do some people get it and why is it that some people don’t. The sooner we understand that,” said Lonnie, “the sooner we will be able to address treatment – better treatment – options for people.”
She continued, “Looking at the genetics of the illness and the way 23andMe is doing it &#8211; getting a broad base of people to participate in the research &#8211; is extremely important to finding a cure. Then all the added things 23andMe does with regards to the person &#8211; giving them information about their personal health history and how to keep them healthy aside from Parkinson’s, because what people forget is that people with Parkinson’s don’t just have Parkinson’s, they have a lot of other illnesses. They may have hypertension, they may have diabetes. They could have a lot of other things which agitate the Parkinson’s that they have to live with. So getting all that information back about what works best for you on an individual basis … is very important. It’s a wonderful thing that 23andMe has done, trying to partner with other researchers around the country to try to answer some of these complex questions.”
I left Arizona feeling inspired, full of gratitude and hope for the future of Parkinson’s research. When I was a neuroscientist at Stanford doing brain imaging research I never could have imagined that one day I would be working with Muhammad Ali on a video project. But there is no doubt in my mind that this video, and Muhammad and Lonnie’s involvement with 23andMe, will push 23andMe’s Parkinson’s research to new heights. Parkinson’s disease can be devastating for those with the illness, but sometimes we forget that such a daunting diagnosis can also inspire great courage.
In this job working with the Parkinson’s community, I am continually awed by the reservoir of spirit found among those facing the disease. Just as Muhammad Ali inspired and continues to inspire generations of people with his courage and spirit, those with Parkinson’s who are bound together to fight this disease can inspire us all.
Learn more and see the video at <a href="https://www.23andme.com/pd" target="_blank" rel="noopener noreferrer">www.23andme.com/pd</a>

23andAli

<img decoding="async" class="alignright size-medium wp-image-10750" title="top10ten" src="https://blog-api.23andme.com/wp-content/uploads/2011/12/top10ten-266x300.jpg" alt="" width="200" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/12/top10ten-266x300.jpg 266w, https://blogcms.23andme.com/wp-content/uploads/2011/12/top10ten.jpg 306w" sizes="(max-width: 266px) 100vw, 266px" />
We thought 2010 would be hard to top but we’re happy to say that 2011 has been even better. Scientists uncovered new insights into serious conditions like type 2 diabetes and autoimmune disorders as well as traits like iris patterns. New research has also improved our understanding of the genetics of obesity, a condition that affects nearly two-thirds of Americans. And we ourselves contributed even more to the understanding of Parkinson’s disease while delving into areas that researchers traditionally neglect.
All this and much more happened in 2011 and so this list represents just a snapshot of some of the most intriguing developments.
1. The genetics of Parkinson’s disease gets a little clearer and novel breakthroughs may contribute to potential new treatments.
<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-8774" title="cell-culture_petri-dish" src="https://blog-api.23andme.com/wp-content/uploads/2011/03/cell-culture_petri-dish-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/03/cell-culture_petri-dish-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2011/03/cell-culture_petri-dish-271x271.jpg 271w" sizes="auto, (max-width: 150px) 100vw, 150px" />
In June, 23andMe reported discovering novel genetic variants associated with Parkinson’s disease and in the process also replicated nearly two dozen previously reported associations. Later in the year, we also announced the discovery of <a href="https://blog.23andme.com/articles/parkinsons-discoveries" target="_blank" rel="noopener">a potential protective genetic factor</a> against Parkinson’s disease in the SGK1 gene. We’re not the only ones making progress &#8212; in March, scientists at Stanford announced that they’d successfully created <a href="https://blog.23andme.com/articles/milestones-in-the-fight-against-parkinsons-disease" target="_blank" rel="noopener">a line of cells</a> that exhibits biochemical properties of the disease in the petri dish. Together, these discoveries offer hope in the quest for determining causes and developing possible cures.
2. Genetic factors for type 2 diabetes are shared between populations of South Asian and European descent &#8212; but perhaps not equally.
<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-10069" title="IndianWoman(iStockblog) copy" src="https://blog-api.23andme.com/wp-content/uploads/2011/10/IndianWomaniStockblog-copy-150x150.jpg" alt="" width="150" height="150">
People with South Asian ancestry develop type 2 diabetes at much higher rates than people with European ancestry, but relatively little is known about the genetic factors influencing this increased risk in South Asians. A recent study of nearly 60,000 people of South Asian descent <a href="https://blog.23andme.com/articles/snpwatch-genetic-variants-associated-with-type-2-diabetes-in-south-asians-and-europeans" target="_blank" rel="noopener">identified several genetic variants linked to type 2 diabetes</a>. These variants also seem to be associated with the disease in Europeans, and similarly, genetic factors previously identified in Europeans appeared to be linked to the disease in South Asians. Most of these genetic variants, however, showed stronger effects in one population than the other.
3. Genetic associations with obesity differ depending on age.
<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-1483" title="medicalscale" src="https://blog-api.23andme.com/wp-content/uploads/2008/09/medicalscale-150x150.jpg" alt="" width="150" height="150">
Genetic variants in the FTO gene have been linked repeatedly to risk for obesity, but new research is also revealing the complex interplay between these variants and non-genetic factors. In a <a href="https://blog.23andme.com/articles/snpwatch-association-between-fto-variant-and-obesity-depends-on-age-and-impacts-development" target="_blank" rel="noopener">study published last February</a>, researchers found that the same version of an obesity-linked SNP had the opposite association with BMI in very young children than it did in older children. The association corresponds with a difference in a developmental marker known as “adiposity rebound”. The timing of adiposity rebound has been linked to obesity and related diseases later in life.
4. Genetic variation is in the eye &#8212; or iris patterns &#8212; of the beholder.
<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-1553" title="browneyes" src="https://blog-api.23andme.com/wp-content/uploads/2008/10/browneyes-150x150.jpg" alt="" width="150" height="150">
Rings, spots and flecks of color, lines and shapes and furrows – although no two irises are the same, what causes these differences? Thanks to an Australian study of nearly 3,000 individuals, we now know that at least <a href="https://blog.23andme.com/articles/snpwatch-genetic-variation-is-in-the-eye-of-the-beholder" target="_blank" rel="noopener">a few specific genetic variants contribute to the appearance of certain iris patterns</a> such as “crypts”, “furrow contractions”, and pigmented rings. So go on, take a look in the mirror and see what kind of patterns you have in your iris and your genetics!
5. Sex matters in genetic association studies.
<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-9756" title="diversity(iStockBlog)" src="https://blog-api.23andme.com/wp-content/uploads/2011/09/diversityiStockBlog-150x150.jpg" alt="" width="150" height="150">
Many diseases occur more frequently in one sex than the other but most genetic research doesn’t look at these differences, potentially missing genetic factors that have opposite effects in men and women or ones that only have an effect in one sex or the other. A Stanford research group analyzed data from one of the largest and first genome-wide association studies and found several genetic variants associated with Crohn’s disease and coronary heart disease in a sex-specific manner. They suggest that many more sex-specific factors are waiting to be identified.
6. His and Hers: Genetic factors underlying prostate cancer differ in different ethnicities and genetic factors influence breast density in women.
<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-4873" title="prostatemen" src="https://blog-api.23andme.com/wp-content/uploads/2009/09/prostatemen-150x150.jpg" alt="" width="150" height="150">
New studies continue to increase our understanding of prostate cancer and breast cancer, two of the most common cancers in men and women, respectively. Women with high mammographic density have four to five times higher risk for breast cancer and in January, researchers reported a <a href="https://blog.23andme.com/articles/snpwatch-researchers-identify-variant-associated-with-breast-density" target="_blank" rel="noopener">genetic variant linked to both mammographic breast density and breast cancer risk in women</a>. For prostate cancer, we know quite a bit about genetic factors in Europeans but far less about those relevant for African Americans. In May, one of the largest studies of prostate cancer in African Americans found that <a href="https://blog.23andme.com/articles/ethnicity-matters-in-research-a-case-study-in-prostate-cancer" target="_blank" rel="noopener">only half of the genetic factors</a> linked to prostate cancer in people of European descent are linked to the cancer in African Americans.
7. 23andMe initiatives old and new prove the power of participant-driven research.
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In 2011, we launched two new research initiatives. The first, focused on myeloproliferative neoplasms, continues our commitment to advancing knowledge of rare diseases using our unique research platform. The second initiative, Roots into the Future, aims to improve our understanding of the connection between DNA and disease in African Americans, a population that is significantly understudied. We’ve been enrolling participants into both of these initiatives at an incredible pace and are extremely excited to begin making important discoveries with their help. And as our Sarcoma Community Night showed us, our research participants are among the most passionate and inspiring people in the world.
8. Scientists discover new genetic factors for migraine susceptibility and 23andMe replicates the findings in days.
<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-5157" title="migraine" src="https://blog-api.23andme.com/wp-content/uploads/2009/10/migraine-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/10/migraine-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2009/10/migraine-271x271.jpg 271w" sizes="auto, (max-width: 150px) 100vw, 150px" />
In June, the largest migraine study to date reported three genetic variants associated with risk for this debilitating disorder. It turns out that 23andMe’s database contains thousands of people who suffer from migraines and we were able to replicate the new study’s findings in a matter of days. This is just a small example of the power and speed of our research platform as shown by a paper we published in August replicating more than 180 genetic associations for three dozen different medical conditions in a fraction of the time it would take using the traditional research model.
9. Many genetic factors are shared across multiple autoimmune disorders.
<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-5013" title="dnaoragami" src="https://blog-api.23andme.com/wp-content/uploads/2009/10/dnaoragami-150x150.jpg" alt="" width="150" height="150">
Numerous studies have pinpointed genetic factors associated with autoimmune disorders such as rheumatoid arthritis, multiple sclerosis, lupus, and psoriasis to name a few. Some of these genetic factors pop up over and over again, raising the question of whether these disorders are genetically interconnected. A study published in August took a closer look at this question by examining more than 100 genetic variants previously linked to autoimmune disorders. The result: nearly half of these variants are associated with at least two different conditions.
10. New insights into our shared African ancestry, both ancient and recent.
<img loading="lazy" decoding="async" class="alignright size-thumbnail wp-image-8628" title="Hadza-hunter" src="https://blog-api.23andme.com/wp-content/uploads/2011/03/Hadza-hunter-150x150.jpg" alt="" width="150" height="150" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/03/Hadza-hunter-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2011/03/Hadza-hunter-271x271.jpg 271w" sizes="auto, (max-width: 150px) 100vw, 150px" />
Prevailing scientific thought pins the origins of the human species in eastern Africa, but new research published this past March suggests a different story. By measuring genetic variation from different populations around Africa, researchers at Stanford, UCSF and 23andMe found evidence that our ancestral origins may actually lie in southern Africa. And for many people of European descent, their African ancestral origins may be much closer than that. Scientists at 23andMe examined the genetic ancestry of nearly 80,000 individuals who are likely to identify as entirely of European ancestry and discovered that between three and four percent have some amount of “<a href="https://blog.23andme.com/articles/hidden-african-ancestry" target="_blank" rel="noopener">hidden African ancestry</a>”.

Our Top 10 for 2011

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It&#8217;s been an exciting year for research on Parkinson&#8217;s disease. In March, scientists from Stanford were able to <a href="https://blog.23andme.com/articles/scientists-score-a-breakthrough-with-parkinsons-in-a-petri-dish#more-8772" target="_blank" rel="noopener">recreate features of the disease in a petri dish</a> using cells from a Parkinson&#8217;s patient. In June, we published a paper in PLoS Genetics detailing our discovery of two novel genetic associations with Parkinson&#8217;s. Now, we&#8217;ve also identified a genetic factor in a gene called SGK1 that may protect against the disease.
This preliminary finding comes as a result of our innovative research and recruitment platform, which in just a few years has assembled the largest single genotyped group of Parkinson&#8217;s patients in the world. Of the 125,000 individuals in 23andMe&#8217;s database, there are more than 6,000 with Parkinson’s disease.
Even more astonishing is the fact that we can collect large cohorts of people who share similar genetics, regardless of their health status. Most studies can only recruit individuals who have a disease, but our database allowed us to identify the world&#8217;s largest cohort of people carrying the G2019S variant in the LRRK2 gene. Roughly 1 in 10,000 people have this variant, which is associated with a 50% lifetime risk of Parkinson&#8217;s compared to about 1% in the general population. But within our database there are many people with this high risk variant who are at an age when they should have developed the disease but have not. By comparing these people to those with the variant who did develop Parkinson&#8217;s, we were able to discover the potentially protective nature of SGK1.
Watch 23andMe CEO and co-founder Anne Wojcicki discuss this finding in conversation with WIRED editor Thomas Goetz at the Web 2.0 conference.
https://www.youtube.com/watch?v=9fMeb9urMhw
With generous support from <a href="http://www.michaeljfox.org/" target="_blank" rel="noopener">The Michael J. Fox Foundation</a> (MJFF), we&#8217;ve partnered with <a href="http://www.scripps.edu/" target="_blank" rel="noopener">The Scripps Research Institute</a> to study the connection between SGK1 and LRRK2 further to see if the finding could lead to a potential new treatment for Parkinson&#8217;s disease. Said Todd Sherer, CEO of MJFF, &#8220;The SGK1 discovery, while still early-stage, is a promising outcome of this unique research platform&#8230; We are eager to see the results of the continued investigation of SGK1 by Scripps.&#8221;
Of course, none of this would be possible without our amazing research participants. Although we are well on our way to 10,000, we still need the support of thousands more to reach our goal. If you or someone you know has Parkinson&#8217;s disease, we encourage you to join the community. Participating is easy &#8212; just visit <a href="https://www.23andme.com/pd" target="_blank" rel="noopener">https://www.23andme.com/pd</a> to get involved!
Watch Paula, who has Parkinson&#8217;s disease, tell her story. (This video was first shown at  Health 2.0 San Francisco  earlier this fall.)
<iframe loading="lazy" title="23andMe Presents Patient Perspective on Parkinson&#039;s Research" width="500" height="281" src="https://www.youtube.com/embed/fmnrG9MoDx8?feature=oembed" frameborder="0" allow="accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture; web-share" referrerpolicy="strict-origin-when-cross-origin" allowfullscreen></iframe>
This most recent finding is just the tip of the iceberg of what is possible when individuals come together to contribute to research.  We continue to be inspired, not just by the progress we&#8217;re making, but by people like Paula, who are fighting every day with grace and courage and working towards making the world better for people with Parkinson&#8217;s.
Learn more at <a href="https://www.23andme.com/pd" target="_blank" rel="noopener">https://www.23andme.com/pd/</a>.

Milestones in the Fight Against Parkinson’s Disease

Even though they aren&#8217;t self-lacing and don&#8217;t come with a hoverboard, the limited-production Nike Mags – Marty McFly’s fly shoes from the 1989 movie Back to the Future II – are still flying off the shelves as part of the company’s effort to raise money for Parkinson’s disease research.
Since September 8th Nike began auctioning off 150 of the shoes a day on eBay with the money going to <a href="http://www.michaeljfox.org/">The Michael J. Fox Foundation</a>. The sale ends on September 18th.
23andMe co-founder Anne Wojcicki and her husband Google co-founder Sergey Brin will match all donations to the foundation, up to $50 million, through the end of 2012.
Fox, who played McFly in the three Back to the Future movies, said the campaign has brought together three passionate audiences – the Parkinson’s community, “sneakerheads,” and fans of the movies.
“With their support we can accelerate our objective of finding a cure for Parkinson’s,” Fox said.
For more than two years 23andMe has worked with the Michael J. Fox Foundation, as well as other Parkinson’s groups to enroll 10,000 patients into our <a href="https://www.23andme.com/pd/">Parkinson’s Research Community</a>. We’re more than half way there already and we’ve already made some important breakthroughs finding <a href="https://www.23andme.com/about/press/pd_discoveries_plos_62311/">two new genetic associations</a> with the diseases and confirming 20 previously identified associations.
Even with the progress we’ve made so far, we still need to enroll another 4,200 people to reach our goal. If you, or someone you know has Parkinson’s and is willing to participate in this exciting new research revolution please consider signing up.

McFly’s Shoes to Help Fight Parkinson’s

<img loading="lazy" decoding="async" class="alignleft wp-image-9002 size-medium" title="l.tif" src="http://35.88.189.111/wp-content/uploads/2011/04/Birthday-Cake--229x300.jpg" alt="" width="229" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/04/Birthday-Cake--229x300.jpg 229w, https://blogcms.23andme.com/wp-content/uploads/2011/04/Birthday-Cake-.jpg 605w" sizes="auto, (max-width: 229px) 100vw, 229px" />
The typical five year-old is pretty confident, filled with energy and imagination. Maybe a little loud.
Yesterday, 23andMe turned five.
We’re brimming with vigor and vision. Still a little brash.
<a href="../articles/the-power-of-we/" target="_blank" rel="noopener">Conceived</a> with the goal of allowing people to explore their genetic information, 23andMe uses new tools that allow people to gain insight into their ancestry, genealogy and health.
Who knew that would be so <a href="https://www.nytimes.com/2011/01/18/science/18tier.html?scp=9&amp;sq=genetic%20tests&amp;st=cse" target="_blank" rel="noopener">controversial</a>?
On top of giving people access to their genetic information, we’ve invited them to join our new research paradigm. This idea inspired the vision for creating the company in the first place. Build an ever-growing database of genetic information to accelerate research and engage people in that exploration.
In the five years we’ve been in business we’ve done just that.
Tens of thousands of people have sifted through their genetic information at 23andMe.
They’ve found everything from whether they’ve got a “<a href="https://www.23andme.com/gen101/variation/speed/" target="_blank" rel="noopener">sprinter’s gene</a>,” to a friend in Norway who’s actually a fifth cousin to whether they have an elevated genetic risk for breast cancer. 
 
The draw of finding out more about ourselves individually empowers us to find out more about ourselves communally.
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Our first <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000993" target="_blank" rel="noopener">proof-of-concept study</a> uncovered associations with common traits like hair curl, eye color, and whether you can smell the by-products of asparagus. Since then, we’ve presented <a href="../articles/23andme-research-team-presents-findings-at-international-human-genetics-meeting/" target="_blank" rel="noopener">preliminary findings</a> from our studies uncovering novel genetic links to childhood and adult infections, Parkinson’s disease, and hair traits. And our studies have replicated more than 100 previously identified genetic associations for dozens of common diseases and medical conditions. All in a <a href="https://www.wired.com/magazine/2010/06/ff_sergeys_search/" target="_blank" rel="noopener">fraction of the time</a> it typically takes to conduct such studies.
We are still enrolling people in our new<a href="https://www.23andme.com/sarcoma/" target="_blank" rel="noopener"> Sarcoma community</a>. We plan to combine genetic information with survey data to detect patterns for better understanding the biology of sarcoma.
Our <a href="https://www.23andme.com/research/" target="_blank" rel="noopener">research initiatives</a> have already begun to yield results.
Earlier this month at a workshop sponsored by the <a href="http://www.ninds.nih.gov/index.htm" target="_blank" rel="noopener">National Institute for Neurological Disorders and Stroke</a> (NINDS) in Washington, D.C. our scientists presented more discoveries from our growing Parkinson’s Disease Research Initiative. Working with our partners – the <a href="http://www.thepi.org/" target="_blank" rel="noopener">Parkinson’s Institute</a> and the <a href="http://www.michaeljfox.org/" target="_blank" rel="noopener">Michael J. Fox Foundation</a>, among others – and the people who have volunteered to be part of this ongoing research we conducted the largest genome-wide association study of Parkinson’s based on a single cohort. Almost 3,500 people with Parkinson’s participated and another 30,000 people were included as part of a control group. The number of people with Parkinson&#8217;s who&#8217;ve now enrolled in our on-going study has grown to about 5,000. We hope to reach 10,000.
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The study identified a substantial genetic component underlying the development of the debilitating disease. The work also identified two new genetic variants associated with Parkinson’s and confirmed 20 other genetic associations previously identified including variants near the LRRK2, GBA, SNCA, MAPT, GAK, and the HLA genes. We are planning to publish these results soon.
23andMe scientist Dr. Chuong Do said the work in this study indicates the heritability of Parkinson’s disease is at least 25 percent.
But the work has really only scratched the surface. The next step is collaborating with several other groups and combining data sets to look at perhaps as many as 15,000 cases. Do feels confident that additional novel variants will be found that could help shed more light on the disease.
In the meantime, 23andMe customers now can access updated information about the genetics of Parkinson’s disease in their accounts. We have added four well-established genetic associations to the calculation of risk for Parkinson’s disease, of which three are also applicable to East Asian populations. We plan to update the Parkinson’s Disease report again soon once our own study is published.
Our first five years have been exciting, inspiring, and rewarding. Thank you to all of our customers, collaborators, and research contributors.
We’re still discovering the power of genetics to inform and inspire both intellectual and personal exploration. We hope you’ll continue on this journey with us.
<img loading="lazy" decoding="async" class="aligncenter wp-image-9008 size-full" title="2011company_photo" src="http://35.88.189.111/wp-content/uploads/2011/04/2011company_photo.jpg" alt="" width="500" height="321" srcset="https://blogcms.23andme.com/wp-content/uploads/2011/04/2011company_photo.jpg 500w, https://blogcms.23andme.com/wp-content/uploads/2011/04/2011company_photo-300x193.jpg 300w" sizes="auto, (max-width: 500px) 100vw, 500px" />

Parkinson's Disease — Page 8