With assorted schwag in hand, our team of elite 23andMers headed to Burbank last weekend to pass out a few free kits, some t-shirts and mingle with some of the most committed genealogists on the planet.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-13778" title="MikeatJamboree" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/MikeatJamboree-300x172.jpg" alt="" width="300" height="172" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/MikeatJamboree-300x172.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/06/MikeatJamboree-1180x678.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2012/06/MikeatJamboree-768x442.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/06/MikeatJamboree-1024x589.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2012/06/MikeatJamboree-880x506.jpg 880w" sizes="auto, (max-width: 300px) 100vw, 300px" />Mike Macpherson ready to answer a few ancestry questions.
This year’s Southern California Genealogy Jamboree drew more than 1,700 people over three days. There are just a handful of other events around the country that attract such a large number of people who are so knowledgeable and focused on learning about their ancestry. It’s not the first time we’ve been there, but it was the first time we brought a posse.
While there, we were lucky to learn a little about what these ancestry experts wanted out of 23andMe’s tools. In turn, we gave them a sneak peek of a host of new ancestry features we’ll be launching in a test format in the coming weeks. 
 
Mike Macpherson, one of our scientists, was on hand to answer questions. Mike helped develop this turbo charged package of new ancestry features we’ll soon be launching in a beta test. He was also there to participate on a panel discussion during the event put on by the International Society of Genetic Genealogy (ISOGG). With him on the panel were 23andMe Ancestry Ambassador CeCe Moore, whose<a href="http://www.yourgeneticgenealogist.com/"> blog</a> is a go-to source for interesting stories and information about the use of genetics in genealogy, as well as Bennett Greenspan from Family Tree DNA, and Katherine Borges, the co-founder and director of ISOGG.
During the three days in Burbank, our team found that even among these experts at hunting down family histories – people who’ve focused for decades on assembling the lost stories of their ancestry – there were some folks who were new to the <a href="https://www.nature.com/news/ancestry-testing-goes-for-pinpoint-accuracy-1.10785" target="_blank" rel="noopener noreferrer">power of genetic genealogy.</a>
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-13779" title="23andMe Winner Phyllis" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/23andMe-Winner-Phyllis-300x225.jpg" alt="" width="300" height="225" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/23andMe-Winner-Phyllis-300x225.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/06/23andMe-Winner-Phyllis.jpg 612w" sizes="auto, (max-width: 300px) 100vw, 300px" />Phyllis Kinzle, one of the lucky winners of a free kit at the Jamboree, said, &#8220;It&#8217;s a good time to start this new adventure!&#8221;
With Mike to help answer some of those folks’ questions were creative manager Melissa del Sol, public relations manager Catherine Afarian, and our social media guru Rebecca Wolpinsky. During the conference the team, along with CeCe, hung out and filled in the attendees about what DNA could do to help them fill in the gaps in their ancestry hunts.
They let folks know that now with more than 150,000 genotyped customers; we have the world’s largest database for ancestry. With a full range of ancestry tools that take advantage of autosomal DNA as well as yDNA and mitochondrial DNA, 23andMe can give results not just from maternal and paternal lines but from all of your ancestors. And we do all of that, along with providing health results, for <a href="https://www.23andme.com/store/cart/" target="_blank" rel="noopener noreferrer">one price.</a>

23andMe Blog

23andMe Blog Team

23andMe at the Genealogy Jamboree

Check out <a title="Three Degrees of Genetic Separation" href="https://blog.23andme.com/ancestry-2/three-genetic-degrees-of-separation/">this post</a> for an illustration of the three degrees of separation between guests on Finding Your Roots.
When we learn about our ancestors, who they were, and where they came from, the discoveries become part of how we define ourselves and understand ourselves as unique. The PBS series Finding Your Roots has taken this further, showing us how much we share with others and how interconnected our stories are.
<img loading="lazy" decoding="async" class="aligncenter size-medium wp-image-13441" title="MikeandSkpforBlog" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/MikeandSkpforBlog-300x250.jpg" alt="" width="300" height="250" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/MikeandSkpforBlog-300x250.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2012/06/MikeandSkpforBlog.jpg 393w" sizes="auto, (max-width: 300px) 100vw, 300px" />23andMe Scientist Mike Macpherson going over connections between guests with Prof. Henry Louis Gates, Jr. and a Finding Your Roots producer.
<h2>Finding Your Roots</h2>
This has been a theme of the 10-part series, something that the show’s host, Professor Henry Louis Gates, Jr., has repeatedly repeated—that despite our differences, whether racial or cultural, Americans are more interconnected than we know.
It isn’t just that our stories share parallels but that the connections run deep and can be seen in our DNA. It’s ironic that as the world’s population has grown exponentially in the last 500 years – from about half a billion to now seven billion – we are closer and more connected.
During the show&#8217;s filming, Professor Gates visited 23andMe and talked to scientists Mike Macpherson and Joanna Mountain, both of whom served as consultants.
<h2>Connecting People</h2>
At one point, Macpherson taped up photographs of the roughly two dozen guests who appeared in Finding Your Roots. Then, he sketched out the genetic connections that linked this seemingly random collection of people.
This was the first time someone demonstrated the genetic connectivity of any two people on Earth. Macpherson made some surprising links that connected, for example, Martha Stewart to Samuel L. Jackson and Barbara Walters to the Imam Yasir Qadhi.
Unlike previous examples that relied on social connections – friends of friends of friends – this connection is through cousins matched within 23andMe&#8217;s database of over 150,000 people.
<h2>Social Connections versus Genetic Ones</h2>
This wasn’t just a parlor game. Indeed, Stanley Milgram first wrote about the notion that any two people—a cop in New York and a street vendor in Mumbai, say—could be connected through five other people based on experiments he conducted in the late 1960s. It’s a little more complicated than Milgram theorized, but he got the gist right.
<img loading="lazy" decoding="async" class="aligncenter size-full wp-image-13443" title="MikeInterconnection" src="https://blog-api.23andme.com/wp-content/uploads/2012/06/MikeInterconnection.jpg" alt="" width="414" height="167" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/06/MikeInterconnection.jpg 414w, https://blogcms.23andme.com/wp-content/uploads/2012/06/MikeInterconnection-300x121.jpg 300w" sizes="auto, (max-width: 414px) 100vw, 414px" />23andMe scientist Mike Macpherson sketching connections between the guests on Finding Your Roots as Prof. Gates looks on.
These previous theories of connectivity focused on social connections, the idea that we are all – all seven billion of us – linked to each other by six degrees of separation.
This connectivity theory even spawned a game named after one of Gates’ guests,  <a href="http://oracleofbacon.org/">“Six Degrees of Kevin Bacon.”</a> The game links any actor to Kevin Bacon by five other performers. Bacon – whose wife Kyra Sedgewick was also on the show – said for a long time he<a href="http://www.nbcchicago.com/video/#%21/news/business/Kevin-Bacon-Explains-Six-Degrees-Story/131838958"> hated that his name was the punchline for a joke</a>. But he has since embraced it and is using the idea of social connections <a href="http://www.sixdegrees.org/">to link people to worthy causes</a>.
More recently, <a href="https://www.nytimes.com/2011/11/22/technology/between-you-and-me-4-74-degrees.html?_r=3&amp;scp=1&amp;sq=4.74&amp;st=cse">Facebook</a> and LinkedIn have shown that just four “connections” could link any two people together.
Macpherson connected the Finding Your Roots guests via a much shorter genetic chain. Any two people are connected through just one or two other individuals.
<h2>Why is this a revelation?</h2>
It’s new because this isn’t the notion that you are connected to someone else because of who you know. It’s the notion that you are connected to someone because of who you are related to.
This is a manifestation of human history and human migration over the last 500 years. 
<iframe loading="lazy" src="https://www.youtube.com/embed/F-zRXHAo4-U" width="420" height="315" frameborder="0"></iframe>
People are no longer isolated by geography and so the differences between people are smaller than in the past .
Perhaps in no other place has the convergence of people of different cultures and histories been as dramatic as the Americas. And while the clash of cultures and histories has been both painful and brutal at times, it is what forged our history more than anything else, Gates argues.
“I’ve always thought that it was that story of America,” said political commentator Linda Chavez in the last episode in the series.
People came here from all over the world, some voluntary and some involuntary, and mixed, she said, “and that’s made us stronger.”
This post by 23andMe Content Editor Scott Hadly and 23andMe Senior Director of Research Joanna Mountain first appeared last week on <a href="https://www.pbs.org/wnet/finding-your-roots/" target="_blank" rel="noopener noreferrer">PBS&#8217;s Finding Your Roots website</a>. It was one of a series of posts by 23andMe. Dr. Mountain was a consultant for the the 10-part series.

Make That Three Degrees of Separation

<img loading="lazy" decoding="async" class="aligncenter size-full wp-image-13429" title="ASCO image" src="https://blog-api.23andme.com/wp-content/uploads/2012/05/ASCO-image.jpg" alt="" width="557" height="102" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/05/ASCO-image.jpg 557w, https://blogcms.23andme.com/wp-content/uploads/2012/05/ASCO-image-300x55.jpg 300w" sizes="auto, (max-width: 557px) 100vw, 557px" />
Starting today cancer researchers will be gathering in Chicago at the meeting of the<a href="http://www.asco.org/"> American Society of Clinical Oncology</a>.
Researchers and doctors at the annual meeting – the world’s largest oncology conference – will hear about the most promising drugs being developed to fight cancer. They’ll spend five days learning about the new science around a vast array of cancers, and discuss the newest therapies as well as the latest and most innovative clinical trials. They’ll wrestle with broader issues on ethics and hunt out presentations about the most successful cancer prevention.
But this year we hope that a few will also take notice of a new approach to cancer research being pioneered by 23andMe.
Along with our scientific advisors – who include <a href="http://doctors.dana-farber.org/directory/profile.asp?dbase=main&amp;setsize=16&amp;pgt=George+D%2E+Demetri%2C+MD&amp;picture_id=0000273&amp;grouptype_typeid_data=1&amp;gs=c&amp;nxtfmt=r&amp;display=Y&amp;lookup=Y&amp;oldurl=Y&amp;pict_id=0000273">Drs. George Demetri</a>, Robert Maki, Judy Garber, and Mark Robson, – our very own Dr. Kim Barnholt, the Research Project Manager for both our<a href="https://www.23andme.com/sarcoma/"> Sarcoma</a> and<a href="https://www.23andme.com/mpn/"> Myeloproliferative Neoplasms</a> (MPN) research communities, is attending. Kim will be presenting some of the highlights of our 23andMe’s work on sarcoma.
We’ve been able to recruit almost 1,000 people with these cancers that develop in bone and soft tissue, making our sarcoma research cohort one of the world’s largest. Sarcoma, which strikes about 14,000 people each year, is not one kind of cancer, but many different ones.
The complexity of what turns out to be dozens of subtypes of sarcomas makes treating and studying them difficult. But using web-based tools allows for both quick recruitment and efficient large-scale genome-wide studies of the disease. It also gives people with sarcoma, who might be geographically isolated or far away from cancer research centers, or too sick to travel, an easier way to participate in research.
Kim is most encouraged by the engagement of the community with more than 80 percent of participants having completed important surveys. &nbsp;Last summer, she put together an<a href="https://www.23andme.com/sarcoma/videos/"> evening gathering</a> for the community giving patients a chance to directly interact with her and other scientists at 23andMe, as well as with sarcoma researchers and advocates.
<img loading="lazy" decoding="async" class="aligncenter wp-image-6395 size-full" title="sarcoma-large" src="http://35.88.189.111/wp-content/uploads/2010/04/sarcoma-large.jpg" alt="" width="350" height="289" srcset="https://blogcms.23andme.com/wp-content/uploads/2010/04/sarcoma-large.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2010/04/sarcoma-large-300x248.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
“It’s important for researchers to meet patients,” Kim said recently. “It gives more meaning to what we do. There’s more than just numbers in research. Understanding the personal stories and each person’s journey gives what we do more relevance and meaning, but it also gives us a better picture of the disease. It all goes back to the quality of measurement in research. If you can talk and interact with patients and they have a voice and that is part of the data collection, it improves the what we do. I know it does for my work.”
Kim plans to present some preliminary data in Chicago and report back over the next few days on some of the most interesting presentations.

23andMe at Oncology Conference

Andrew Rubin and Ricardo Villarreal’s film Ride With Larry is about more than a guy with Parkinson’s pedaling across South Dakota.
It&#8217;s about the singular idea that whatever life throws at you the best choice is to live to the fullest.
“I’ll never give up,” Larry Smith says at one point during the film. “I know that this will some day take me, but I’m not going to walk away from life.”<iframe loading="lazy" src="https://www.youtube.com/embed/SNblbb3tyGI" width="560" height="315" frameborder="0"></iframe>
We first heard about Larry when Andrew and Ricardo came through town to interview our CEO Anne Wojcicki and Emily Drabant, who heads up our <a href="https://www.23andme.com/pd/">Parkinson’s Research Community</a>.
Larry is a retired police captain who opened a small town bakery. His example has already inspired his family and the people in his small town of Vermillion. Andrew and Ricardo hope to inspire others with Larry’s story. For Andrew the film is also personal as his own father and a cousin are living with Parkinson’s. He hopes to rally people behind efforts to research the disease, including 23andMe’s own <a href="https://www.23andme.com/pd/">Parkinson’s Research Community</a>.
A few days ago we got wind that “Ride with Larry” was in post-production, along with the note, “Would we like to see a short preview?”
It’s an awesome peek at what the filmmakers have been up to and we&#8217;re grateful that they’ve shared it with us.
Andrew and Ricardo, who are still busy editing, also were gracious enough to answer a few questions.
How is Larry doing since you guys finished up?
<img loading="lazy" decoding="async" class="aligncenter wp-image-12535 size-full" title="AndrewRicardo" src="http://35.88.189.111/wp-content/uploads/2012/04/AndrewRicardo.jpg" alt="" width="525" height="276" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/04/AndrewRicardo.jpg 525w, https://blogcms.23andme.com/wp-content/uploads/2012/04/AndrewRicardo-300x158.jpg 300w" sizes="auto, (max-width: 525px) 100vw, 525px" />
Andrew and Ricardo: Larry is doing great; he is obviously very excited about the film and can&#8217;t wait for it to be finished. Larry has become a small celebrity in his state of South Dakota and continues to inspire his community in many ways, including his determination to get up everyday and bake his famous bread.  Since we finished shooting last summer, Larry also has a new granddaughter.
In terms of his battle with Parkinson&#8217;s, Larry continues to fight.  He  exercises  regularly and this June the people of Vermillion, SD are planning a one day ride in honor of Larry to continue raising awareness for Parkinson&#8217;s.
What have you learned or are most excited about from the experience of shooting this film?
Ricardo: What I learned from shooting this incredible story is that life is so precious and there is no excuse not to enjoy it and live it the best way you can.
Although there&#8217;s no cure for Parkinson&#8217;s yet, we have the power and the choice to live life to the fullest. This experience also taught me that real heroes can be found within ordinary people. You don&#8217;t have to be someone famous, rich, or powerful to be a role model and to make a positive impact in your community.
The excitement about shooting the film is that we have this great opportunity to share this inspiring story with the world and spread Larry&#8217;s message of hope.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-12536" title="Ride with Larry" src="https://blog-api.23andme.com/wp-content/uploads/2012/04/Ride-with-Larry-200x300.jpg" alt="" width="200" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/04/Ride-with-Larry-200x300.jpg 200w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Ride-with-Larry-768x1152.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Ride-with-Larry-683x1024.jpg 683w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Ride-with-Larry-587x880.jpg 587w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Ride-with-Larry-787x1180.jpg 787w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Ride-with-Larry-scaled.jpg 1707w" sizes="auto, (max-width: 200px) 100vw, 200px" />
At the same time,  we are also excited to work together with great organizations that are working hard to find a cure for Parkinson&#8217;s and we want to be part of this movement. Nothing would be more rewarding than to know our film has inspired many people to live better. Additionally, we believe our film can help bring more people to contribute to Parkinson&#8217;s research. Everyone can make a difference, and the more people get involved, the closer we will be to finding a cure.
Andrew: In the process of making this film I learned to embody the very lessons I&#8217;ve witnessed behind the lens of a camera.  Making Ride with Larry has given me perspective.  Every day I watch the struggles of both my father and Larry as they battle Parkinson&#8217;s and Larry&#8217;s wife Betty and my own mother as they confront the difficulties of life as a caretaker.
In the act of telling Larry&#8217;s story, I have come to recognize that in sharing his message, I must also learn it and live it.  The struggles of Parkinson&#8217;s are of the whole body and mind.  They are second-to-second, nerve ending to muscle.  And they choose not to succumb.  If I can face my challenges, no matter how small or large, with the gift of perspective, then I know I can rise to meet them.
It has been amazing not just to be a witness to Larry&#8217;s victory, but to be a part of his ride.  The next exciting part of this journey will be in sharing this story with the world and working to get as many people as possible involved in the Parkinson&#8217;s community and the search for a cure.
What&#8217;s next?
Ricardo: With &#8220;Ride with Larry&#8221;, the next thing is just around the corner: to show this film to audiences everywhere and to grow this movement.

Ride With Larry

In an effort to extend the state’s privacy protections to people’s genetic material, California State Senator <a href="http://dist20.casen.govoffice.com/">Alex Padilla</a> D-Pacoima recently introduced the California Genetic Information Privacy Act.
Last year, California Gov. Jerry Brown signed into law <a href="../2011/09/07/california-governor-signs-law-to-protect-against-genetic-discrimination/">another bill authored</a> by Padilla that extended the state’s anti-discrimination laws to bar discrimination based on genetic information.
The bill introduced earlier this year, <a href="http://dist20.casen.govoffice.com/index.asp?Type=B_PR&amp;SEC=%7B5EACFA15-EA6B-41D8-9711-C030F9FAD5EE%7D&amp;DE=%7B84E67402-17EA-4BF9-8952-2F3FED2DEEC0%7D">Senate Bill 1267</a>, would prevent the secret collection and testing of a person’s genetic material. Specifically the law would bar collection of genetic material without a person’s written consent. The law would impose criminal and civil penalties for violations.
“SB 1267 would extend California privacy protections to a person’s genetic material and information,” said Senator Padilla. “We have laws to protect the privacy of our financial information, our medical records, and even the books we check out from the local library. We need genetic privacy protections because nothing is more personal than our DNA.”

Proposal to Extend Genetic Privacy Protections in California

If you were facing a daunting diagnosis you would want the news to come from someone like Dr. J. William Langston.
Engaged and intelligent, he has the kind of optimism you don’t expect from a physician who has spent decades working to unravel the complexities of Parkinson’s disease.
<img loading="lazy" decoding="async" class="alignright wp-image-12362 size-medium" title="Langston" src="http://35.88.189.111/wp-content/uploads/2012/04/Langston-253x300.jpg" alt="" width="253" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/04/Langston-253x300.jpg 253w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Langston-741x880.jpg 741w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Langston.jpg 750w" sizes="auto, (max-width: 253px) 100vw, 253px" />
“Things have changed dramatically in that time,” Dr. Langston says, his eyes squinting as he smiles. “There is a lot to be optimistic about.”
Some of those changes are because of the work he’s done. As the Scientific Director, Chief Executive Officer and Founder of the<a href="http://www.thepi.org/"> Parkinson’s Institute</a>, Dr. Langston was recently singled out for his work and awarded the 2012 Robert A. Pritzker Prize for Leadership in Parkinson&#8217;s Research.
After picking up the award in New York, Langston, who also serves on 23andMe’s Parkinson’s Research Community<a href="https://www.23andme.com/pd/#section4"> Scientific Advisory Board</a>, stopped by our office to talk about the state of the science of Parkinson’s and share a little about his career in the process.
In a way, Langston is already the doctor for anyone with Parkinson’s – his contributions to research, treatment and diagnosis of the disease are that important. And those contributions started almost 30 years ago with the famous case of the “Frozen Addicts.”  This fascinating medical mystery, solved by Dr. Langston, involved a handful young people who in a matter of days became debilitated with advanced Parkinson’s symptoms that would normally have taken a patient decades to develop. Langston found that they were all linked to the same batch of synthetic heroin, contaminated with<a href="https://en.wikipedia.org/wiki/MPTP"> MPTP</a>, a neurotoxin that “lasers like a Nike missile on the same nerve cells in the brain that die in Parkinson’s,<a href="https://en.wikipedia.org/wiki/Substantia_nigra"> (in the) substantia nigra</a>,” Dr. Langston said.
“That really revolutionized research because it gave us a model and a way to study neurological cell death in Parkinson’s,” he said.
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-11373" title="researchrevolution-fist" src="https://blog-api.23andme.com/wp-content/uploads/2012/02/researchrevolution-fist-173x300.jpg" alt="" width="173" height="300" />
That work led Langston to found the Parkinson’s Institute, a place where basic research, clinical research and patient care could be done side-by-side. He believes it gives context and perspective for his researchers.
“Anyone working on this disease will feel a sense of urgency, because they see it,” Dr. Langston said.
And in the last 30 years the work has helped produce some of the insights that have significantly changed outcomes for people with Parkinson’s.
Doctors have changed how they use drugs to treat the disease. For a time the problem wasn’t so much that the drugs didn’t work but that side effects would build up to the point where doses would have to be lowered right at the time when they were needed most. Now, doctors are getting much better at calibrating the use of medicine and managing the symptoms of Parkinson’s.
While there have been great leaps in understanding of the disease, insight into its progression and avenues for research into a cure, Dr. Langston pointed out that simply diagnosing Parkinson’s early enough – when symptoms are largely benign – and then using medication to halt or drastically slow its progression, would be a great success. Here he felt researchers are very close.
“Already we are on the cusp of bringing out new drugs that work against these side effects and if you put that together with an early diagnosis, you are looking at really managing the disease and giving people a good life,” said Dr. Langston. “Because those early symptoms are so mild, if you get in there and halt it at that point that’s almost as good as a cure.”
This, in part, is why finding the early indicators of the disease is so important. 
When he first started his association with 23andMe, he would get questions from those who wondered why you would want to know if you had a genetic risk for Parkinson’s.
“I hear that less and less I think because 23andMe is helping to change that,” he said. “People see value in it. Knowledge is power. The more you know and understand the more you can do.”
Beyond looking at genetics there are other early indicators. His team is looking at things like autonomic innervation of the heart and REM sleep patterns, or loss of the sense of smell as early indicators for the disease.
“It’s a major focus of the research to find the markers before you have any disability,” he said. “We’re hoping that 23andMe will be part of this effort to find the tools where we can pick this up.”
<img loading="lazy" decoding="async" class="alignright size-medium wp-image-12363" title="Pritzker-photo" src="https://blog-api.23andme.com/wp-content/uploads/2012/04/Pritzker-photo-254x300.jpg" alt="" width="254" height="300" srcset="https://blogcms.23andme.com/wp-content/uploads/2012/04/Pritzker-photo-254x300.jpg 254w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Pritzker-photo-768x906.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Pritzker-photo-868x1024.jpg 868w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Pritzker-photo-746x880.jpg 746w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Pritzker-photo-1000x1180.jpg 1000w, https://blogcms.23andme.com/wp-content/uploads/2012/04/Pritzker-photo.jpg 2000w" sizes="auto, (max-width: 254px) 100vw, 254px" />
But of course, Dr. Langston isn’t satisfied with merely managing the symptoms of the disease; he’d like to cure it. Here, too, he is very optimistic saying what we are so much closer in understanding the underlying causes and pathways for the disease. We are seeing more and more the interrelationship between genetic and environmental factors in the disease, “this notion that your genetics loads the gun and the environment pulls the trigger,” said Dr. Langston.
But even in cases where genetics isn’t involved, genetics research provides great benefit, he said.
“It’s not at all unusual that a rare genetic form turns out to be hugely informative for the common sporadic form of the diseases – we’ve seen this with Alzheimer’s,” said Dr. Langston. “ Each of these new genetic variants, some of which are incredibly rare, have led us to a new protein and that protein leads us to a pathway and that pathway is obviously leading to cell death and Parkinson’s.”
Langston said many of these pathways intersect with mitochondria, the energy packet of cells, and offer giant clues for research into sporadic forms of Parkinson’s.
He sees great promise for what is being done in 23andMe’s Parkinson’s Research Community.
“That is the future, it really is,” he said. “You’ve got the questionnaires and the genetics. I mean most people with PD can tell you if they or someone in their family smoke, but they can’t tell you their genetics. Nobody can unless they’re signed up with 23andMe. Maybe someday everybody will know that, but we’re not there yet. That would be very transformative.”

A Leader in Parkinson’s Research

Today’s post explains what “Sharing Genomes” means at 23andMe, describes several points to consider when sharing, and introduces some exciting new developments in sharing at 23andMe.
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23andMe has revolutionized how people think about DNA. What used to be hidden inside heavy textbooks can now be the subject of cocktail conversation. It’s not just because our unique <a href="https://www.23andme.com">Personal Genome Service</a> ® gives people a chance to explore their own DNA — it’s also because 23andMe represents the first genetics-based social network.
<h6>By “sharing” your genome with other 23andMe customers, you can trace shared ancestry, get a glimpse of the diversity in different people’s genetics, or simply brag about how you’re more Neanderthal than your friends. Through 23andMe you can share a little bit or a lot, or not at all &#8212; it’s up to you. 
 
What can I share at 23andMe?</h6>
<div style="width: 280px; background-color: #eee; border: 1px solid #ccc; margin-left: 15px; padding: 10px; float: right;">Currently, the option without Health reports is called “Basic” sharing on the site, and the option with Health reports is called “Extended” sharing. Within the next two weeks, we plan to relabel these options as follows:
<ul>
<li>&#8220;Basic Sharing&#8221; will be &#8220;Sharing, without health reports&#8221;</li>
<li>&#8220;Extended Sharing&#8221; will be &#8220;Sharing, with health reports&#8221;</li>
</ul>
We want everyone to understand how sharing works at 23andMe and these new labels more clearly describe the distinction between the two options.
</div>
At 23andMe, all customers have the option to share genetic results with others by “<a href="https://www.23andme.com/user/profile/sharing/">Sharing Genomes</a>.”
Sharing genomes always allows you to see each other’s results for ancestry features including Maternal and Paternal Lines, Ancestry Painting, and Global Similarity. You can also use the Compare Genes feature to see how genetically similar you are, and the Family Inheritance feature to see which segments of DNA you might share.
Optionally, you may also choose to see each other’s results for most Health reports.
Currently there is no way to directly view or download each other’s raw genetic data or results for Health reports that require an opt-in. These include BRCA Cancer Mutations (Selected), Parkinson’s Disease, and Alzheimer’s Disease.
<h6>What should I consider before sharing at 23andMe? 
</h6>
The vast majority of things we learn by sharing with others at 23andMe are interesting and positive experiences. For many customers, the ability to compare DNA with friends, close family, and distant cousins is one of the most useful and rewarding aspects of this service. 
However, there are some aspects of sharing that you should be aware of. Within two weeks, we plan to expand our descriptions of sharing throughout the site to address these aspects more fully.
First, some of the information that you directly share can be sensitive, including ancestral origins, family relationships, and health risks. Some people are very comfortable sharing this kind of information, some are not &#8212; it’s a personal choice, and the system allows you to be flexible.
Second, some features, like Compare Genes and Family Inheritance: Advanced, allow you to compare DNA between two people you’re sharing with. Similarly, your shares may compare your DNA with that of people they’re sharing with. This aspect of sharing allows customers to compare people to each other and opens up new genealogical vistas by allowing customers to find evidence of family relationships. These new-found family relationships can be unexpected and sometimes upsetting, but more often they are exciting pieces of a genealogical puzzle.
Third, there is some chance that someone you’re sharing with could learn something about you that you didn’t directly share. For example, if you and someone you’re sharing with have a matching segment of DNA that overlaps a health-associated gene, you might infer something about their genotype on the basis of your own, or vice versa. The one way to be absolutely sure that health information about you is not learned in this way is to abstain from sharing entirely. However, it takes substantial effort to learn things like this.
If you’re unsure, we recommend sharing with people you’re comfortable with. Sharing allows you to use more of the features on the website and adds a new dimension to what you can learn about yourself and your family. Many customers share openly with each other and have only benefited from the experience. As you learn more about genetics and develop a finer sense of the issues involved, you might begin to share more openly yourself.
<h6>New developments in sharing at 23andMe 
</h6>
Today we&#8217;d like to announce a few exciting sharing-related changes coming to some popular 23andMe Labs. Previously in <a href="https://www.23andme.com/you/labs/multi_ibd/">Family Inheritance: Advanced</a>, you could only run comparisons between your shares and close family members. Now, you’ll be able to compare any two of your shares. In Ancestry Finder, you&#8217;ll now be able to view the results for any of your shares.
These changes are expected to go into effect within the next two weeks. We are adding this time period to allow customers to absorb and adjust preferences in advance of the changes. If you’re not comfortable with these capabilities, sharing might not be for you. For others, we hope that these changes enhance your experience at 23andMe and speed genealogical research. Sharing and comparing makes your genetics that much more interesting, and we encourage everyone to share at whatever level they wish.
If you have questions or concerns you’d prefer not to post, please send them to sharing-feedback@23andme.com.

Understanding Sharing at 23andMe

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The term “sarcoma” encompasses over a hundred forms of rare cancers, and the cause behind many of these forms is unknown.
<h6>More on Ewing Sarcoma</h6>
Ewing sarcoma, however, is one sarcoma for which the biology is relatively well understood.
This form is caused by a gene fusion &#8212; a DNA rearrangement resulting in two genes being fused together.  In the case of Ewing sarcoma, the fused genes are EWSR1 on chromosome 22 and typically FLI1 on chromosome 11. Although not much is known about risk factors for Ewing sarcoma, a <a href="https://blog.23andme.com/articles/ewing-sarcoma" target="_" rel="noopener">recent study</a> identified genetic variants associated with higher risk for the condition.
Now, a team of French researchers has uncovered the underlying cause of a new type of sarcoma: a different gene fusion.
<h6>New Research Findings</h6>
In this new study published in <a href="https://www.nature.com/ng/journal/v44/n4/full/ng.1107.html">Nature Genetics</a>, the team led by Olivier Delattre and GaÃ«lle Pierron studied tumors similar to Ewing sarcoma but lacking the EWSR1-FLI1 gene fusion, focusing primarily on bone sarcomas affecting adolescents and young adults. Altogether the researchers examined almost six hundred tumor samples and discovered that twenty-four of these tumors had identical genetic rearrangements &#8212; but a different one than that associated with Ewing sarcoma. This newly-discovered subtype of sarcoma results from a gene fusion between the BCOR and CCNB3 genes, both of which are located on the X chromosome.
<div style="border: 1px solid #000; padding: 10px; font-style: italic; margin-bottom: 15px; width: 200px; float: right; margin-left: 15px;"><img loading="lazy" decoding="async" class="alignleft size-full wp-image-12163" style="float: left; margin-right: 15px;" title="small_23andMe_logo" src="https://blog-api.23andme.com/wp-content/uploads/2012/04/JRBgdIBXKIeVIdETJrxYIw_ttam_logo.jpg" alt="" width="24" height="40" />You can help! If you&#8217;ve been diagnosed with any type of sarcoma, <a href="https://www.23andme.com/sarcoma">join 23andMe&#8217;s Sarcoma Research Community today</a>. Even if you don&#8217;t have sarcoma, you can still contribute to research by <a href="https://www.23andme.com/store">becoming a 23andMe customer</a> and answering surveys.</div>
The two genes involved in this new type of sarcoma both have important biological roles. The BCOR gene encodes a protein that regulates the activity of genes (specifically, genes within a type of stem cell found in bone marrow). Mutations in the BCOR gene can result in serious diseases, such as <a href="http://ghr.nlm.nih.gov/condition/oculofaciocardiodental-syndrome" target="_" rel="noopener">oculofaciocardiodental</a> and <a href="http://ghr.nlm.nih.gov/condition/lenz-microphthalmia-syndrome" target="_" rel="noopener">Lenz microphthalmia</a> syndromes. In addition, BCOR-CCNB3 is not the first documented gene fusion involving BCOR causing disease; when the BCOR gene fuses with the <a href="https://www.ncbi.nlm.nih.gov/pubmed/20807888">RARA</a> gene on chromosome 17, the result is another cancer that affects the blood and bone marrow.
<h6>CCNB3</h6>
The role of the second gene, CCNB3, is somewhat less obvious. This gene encodes a protein expressed only in the testis and is important for the formation of new sperm cells.
The researchers hypothesized that the production of this protein in cells outside of the testis was a key factor in this new type of sarcoma. Using additional experiments, they observed that increased levels of CCNB3 protein led to increased cell proliferation &#8212; a hallmark of cancer &#8212; and that out of nearly one thousand tumor samples, only tumors with the BCOR-CCNB3 gene fusion had high levels of the protein encoded by the CCNB3 gene.
Delattre and Pierron’s findings suggest that the BCOR-CCNB3 gene fusion is directly related to the development of this form of sarcoma. This type of sarcoma may also share other attributes with the better-understood Ewing sarcoma, which results from a different gene fusion. Such new knowledge will hopefully translate into better sarcoma diagnoses and, someday, better treatments.

Gene Fusions Point to a New Type of Sarcoma

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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.

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