{"cache":{"posts_f30bc_0b05f":{"__typename":"RootQueryToPostConnection","nodes":[{"__typename":"Post","id":"cG9zdDoyNDkwMw==","databaseId":24903,"featuredImage":null,"author":null,"date":"2017-01-04T06:00:26","uri":"/articles/our-top-five-from-2016","title_b28e9_bf21a":"Our Top Five from 2016","slug":"our-top-five-from-2016","categories_3cd3e_bf21a":{"__typename":"PostToCategoryConnection","edges":[{"__typename":"PostToCategoryConnectionEdge","node":{"__typename":"Category","id":"dGVybToxMzQ0","name":"Research","slug":"23andme-research","uri":"/category/23andme-research","seo":{"__typename":"TaxonomySEO","title":"Research Archives - 23andMe Blog","opengraphTitle":"Research Archives","metaDesc":"23andMe research unique research model combines genetic and phenotypic information in what is among the largest databases of its kind.","opengraphDescription":"23andMe research unique research model combines genetic and phenotypic information in what is among the largest databases of its kind.","fullHead":"\n\n\n\n\n\n\n\n\n\n\t\n\t\n\t\n\n\n\n"}}}]},"imageOptions":{"__typename":"Post_Imageoptions","featuredImageSquare":{"__typename":"MediaItem","id":"cG9zdDoyNDE4OQ==","altText":"","mediaDetails":{"__typename":"MediaDetails","width":1800,"height":440,"sizes_cad4b_bf21a":[{"__typename":"MediaSize","name":"thumbnail","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-150x150.jpg"},{"__typename":"MediaSize","name":"medium","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-300x73.jpg"},{"__typename":"MediaSize","name":"medium_large","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-768x188.jpg"},{"__typename":"MediaSize","name":"large","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-1024x250.jpg"},{"__typename":"MediaSize","name":"larger","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-880x215.jpg"},{"__typename":"MediaSize","name":"largest","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-1180x288.jpg"},{"__typename":"MediaSize","name":"square_sm","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-271x271.jpg"},{"__typename":"MediaSize","name":"square_md","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-372x372.jpg"},{"__typename":"MediaSize","name":"square_lg","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-574x440.jpg"},{"__typename":"MediaSize","name":"square_xl","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-980x440.jpg"},{"__typename":"MediaSize","name":"wide_sm","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-271x149.jpg"},{"__typename":"MediaSize","name":"wide_md","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-372x204.jpg"},{"__typename":"MediaSize","name":"wide_lg","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-574x315.jpg"},{"__typename":"MediaSize","name":"wide_xl","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440-980x440.jpg"}]},"sourceUrl_772ce_bf21a":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440.jpg","mediaItemUrl":"https://blog-api.23andme.com/wp-content/uploads/2016/08/HealthTraits_A_1800x440.jpg","title_b28e9_bf21a":"Health&Traits_A_1800x440"},"singleTemplateFeaturedImage":"default"},"content_b28e9_bf21a":"

Just before we kick off another year of blogging, it’s worth taking a moment to look back and single out what for us were some of the big stories, breakthroughs or findings in genetics from last year.

Here is our top five. $\"\"$

Diversity

For a very long time, medical research in general has focused largely on people of European ancestry and that is even more apparent with genetic research. Less than five percent of genetic research on disease includes people of African ancestry. In fact most genetic research is focused on people of European ancestry, meaning that we risk missing key scientific discoveries that could benefit people of all ancestries. Last year 23andMe launched two separate efforts meant to help alleviate some of these disparities. Both are NIH-funded studies but they approach the diversity issue in different ways.

Kasia Bryc, a senior scientist and population geneticist at 23andMe, is leading one of the studies that will use admixture mapping to identify genetic variants associated with disease in under-represented populations. This leverages 23andMe’s existing database, which includes a large number of African Americans and Latinos who have mixed ancestry. The second study is the African American African American Sequencing Project that is being lead by Adam Auton, a 23andMe senior scientist and statistical geneticist. This project will help address health research disparities by creating a genetic resource for health research in African Americans that could improve the understanding of diseases in minority populations.

Gene Editing, Again

This is the third year in a row we’ve singled out the innovative technique for specific bits of DNA, called CRISPR. It is a simple and quick way of snipping out deleterious sections of DNA and stitching in “corrected” sections. This offers huge potential for treating diseases or other deleterious conditions. It has already been used to treat sickle cell anemia and lung cancer. But CRISP also presents some serious ethical issues about tampering with human DNA, and there are other issues.

For instance, researchers working on treating HIV found that the virus could quickly develop mutations that resist editing. The findings by researchers at McGill University in Montreal were published back in April. It illustrates the complexity of creating gene therapies with CRISPR. But even with this kind of hurdle, the promise of this technology makes it likely we’ll be hearing more about CRISPR this year.

$\"\"$

Not Depressing

Past efforts to study genetics of major depressive disorder all came up short until last year. It turns out that size matters when it comes to the study of depression. Past efforts were limited by numbers. However a “mega analysis” of data from more than 400,000 people found 17 genetic variants in 15 different genetic regions associated with major depressive disorder.

The study, by scientists from Pfizer, Massachusetts General Hospital and 23andMe identified genes associated with depression and schizophrenia. The study also illustrates the power of big data. While identifying genes associated with the condition is useful to better understand the disease and its causes. It also gives researchers studying the biology of the disease clearer paths to follow, but much work is still needed.

Love and Science

Our year started with the moving story of the married couple, Eric Minikel and Sonia Vallabh. Together they switched careers to become medical researchers and focus all their energy on the study and treatment for prion disease. It is a rare but devastating and fatal genetic condition. It hits the nervous system, impairs brain function, and causes other neurodegenerative symptoms. It typically manifests itself around the age of 50.

Sonia’s mother died of the disease at 52. Sonia inherited the genetic mutation that puts her at a very high risk for the disease. The couple formed a non-profit focused on the disease. They’ve incorporated data from 23andMe in their work and their story has been featured in both the Atlantic and the New Yorker.

The Election

The ascendance of Trump to the U.S. presidency leaves open a lot of questions about the future of government funded research in the US. Not just that even the role of science in setting policy is up in the air. Also unknown is whether the new administration will keep Francis Collins, as director of the NIH. At the helm of the agency since 2009, Collins has helped push the Precision Medicine Initiative, now called “All of Us.” He has deftly navigated the political waters of Washington, but some have publicly pushed for his replacement. Whether he stays or goes, it’s still unknown what if any science initiatives the new administration will champion.

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Perhaps the stories are so interesting because they seem so improbable – tales of ordinary people faced with devastating genetic diseases $\"Research$ grabbing a hold of their destiny, doing their own scientific research and making important discoveries.\n

\nA recent account featured on This American Life by David Epstein, a reporter with the non-profit news site Propublica and the author of The Sports Gene, is the latest in a series of stunning stories that highlight what is possible with the right amount of data, diligence and luck.

Epstein’s story looked at Jill Viles and Priscilla Lopes-Schleip, women who couldn’t seem more different – one a wheelchair-bound Iowan with wilted arms and legs, the other a Canadian Olympian known for her incredible musculature.

They both had mutations in the same gene that causes Dunnigan-type partial lipodystrophy a very rare genetic condition that results in the loss of subcutaneous fat in the limbs. But Jill had one other mutation in that same gene that triggered Emery-Dreifus, a rare type of muscular dystrophy. Epstein focuses on Jill’s incredible do-it-yourself approach to research, first identifying that she had lipodystrophy when she was only an undergraduate, and much later discovering that a connection between that condition and her rare form of muscular dystrophy.

And this story shares some of the same elements as several others we’ve seen recently, in which individuals faced with troubling symptoms and few answers, decide to dive into the science on their own and actually make meaningful discoveries.

One of the more striking stories is a wonderful article that ran last year in The Atlantic by Ed Yong. It focuses on Kim Goodsell, an endurance athlete who taught herself genetics to find out why she suffered from the rare genetic nerve disorder, Charcot-Marie Tooth disease, and another genetic disorder that affects her heart called arrhythmogenic right ventricular cardiomyopathy (ARVC). Smart and driven, Kim, who is not a scientist, was able to figure something out about the conditions that no one else had, that they were connected by mutations in the same gene, LMNA.\n

\nFinally there is the story about Eric Minikel and Sonia Vallabh, a married couple who changed their careers and became researchers after they learned that Sonia would likely develop a devastating and fatal neurodegenerative condition. The pair recently authored a paper making important new findings about prion disease.

There is some debate about whether stories like these represent a harbinger of things or simply edge case exceptions. The efforts featured each of these stories have yet to result in a cure, but each person featured is inspiring for what their efforts represent. Even if these are examples that few others could follow, they do point to the value of enlisting the patient in their own treatment.\n

\nAs Eric Topol pointed out in Ed Yong’s story:

“People have been talking about empowering consumers since there was an Internet, but finally, we’ve reached a point where someone can delve into their condition beyond what the top physicians at the Mayo Clinic could.”

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Researchers often say it’s their love of science that drives their work, but for Eric Minikel and Sonia $\"Eric$ Vallabh it’s their love that propels the science.

The married couple – both are researchers at the Broad Institute and are completing their doctorates at Harvard Medical School – helped to co-author a new paper looking at the genetic risk for developing prion disease, a rare but devastating condition that hits the nervous system, impairs brain function, triggers other neurodegenerative symptoms such as memory loss and insomnia, and ultimately causes death. It’s triggered when a protein misfolds causing clumping in brain tissue, typically manifesting itself around the age of 50.

It’s Personal

For Eric and Sonia this research is personal, as Eric movingly writes in this blog post.

About five years ago, not long after they married, their lives took a sharp turn when Sonia’s mother died at 52. It was only after her mother passed away that Sonia and Eric learned about what killed her – Fatal Familial Insomnia, a form of prion disease. Soon thereafter, Sonia learned that she inherited a genetic mutation, putting her at a very high risk for the disease.

In response, first Sonia, who’d recently graduated from law school at Harvard, and then Eric, a city planner and software engineer, made career changes, dedicating their lives to finding a cure for prion disease. They started working at a lab at Massachusetts General Hospital, took night courses and eventually were accepted at Harvard Medical School. They now work in the Stuart L. Schreiber Research Laboratory at the Broad Institute of MIT and Harvard.

$\"Sonia$

Sonia working in the lab.

Even before this paper they made an impact. A few years ago, the couple formed the non-profit Prion Alliance and Eric started the blog CureFFI, which is a great resource for information about research into prion disease. It also catalogues his education in the science and what motivates him.

Recognition for their Work and Story

Their story has been featured in both the Atlantic and the New Yorker. A joint presentation they did at the American Society of Human Genetics focused on citizen science and crowdsourcing for scientific research.

More recently, Eric developed a statistical method that refuted previous studies suggesting that in families with inherited prion disease, the disease will manifest itself as much as 14 years earlier with each generation. If true that would have been devastating for Sonia, who turned 31 in 2015. However, Eric’s findings also highlight problems with research into other rare diseases, which can suffer from a lack of data or selection bias because the data comes from within the disease communities they study.

The research for this paper – which draws in part from data provided by 23andMe and Exome Aggregation Consortium data from the Broad – is important because it changes assumptions about the risks associated with some of the more than 60 mutations in the PRNP gene that are thought to confer risk for prion disease. In another recently published paper, Harvard’s Robert Green points out that Eric and Sonia’s work doesn’t just shed light on prion; it also highlights the power of sharing genetic data:

“The story of this research stands as a testament to the generosity of unrequited data sharing from thousands of individuals and scientists around the globe and to the unflinching devotion of a young couple to alter their seemingly unalterable genetic destiny,” Green writes.

Real Progress

The study began with the observation that variants in the PRNP gene that have been reported to cause prion disease are at least 30 times more common than expected in the general population. Up until now, many doctors have assumed that all those mutations were associated with a 100 percent risk of developing the disease. However, if all of these mutations were “completely penetrant,” or 100 percent disease-causing, then the number of people developing the disease each year would have to be much higher than what is seen in clinics worldwide. This discrepancy suggested to the researchers that some of these variants could have “incomplete penetrance” or may even have no impact on the disease risk. $\"eric-sonia-in-lab\"$

By comparing the frequency of individual variants in prion disease patients versus the general population, the team found that the variants previously reported to cause prion disease aren’t all created equal — they actually form a spectrum of risk. At one end, some mutations previously reported as disease-causing appear benign, meaning that they do not increase the risk of prion disease above the baseline risk in the general population.

Variants with Different Risk

On the other end, some mutations really do convey a very high risk, upwards of 80-to-90 percent, of developing disease in one’s lifetime. In between, some variants appear to convey an intermediate lifetime risk of, for example, 0.1 or 10 percent. Then, there were some variants for which the data was insufficient to draw conclusions.

According to the researchers, this is great news for some individuals who carry variants that now appear to be low-risk.

“Through our relationship in the patient community, we have met people with several of the mutations that we now believe are low-risk or benign. Some of those people had been told they had a very high risk of disease, so our work changes their prognosis,” said Eric.

Unfortunately, Sonia’s mutation, D178N, isn’t one of those that is low-risk. The new research confirms that the mutation she carries—along with mutations that many others carry—confers a near 100 percent risk for developing prion disease.

“Our work doesn’t change the prognosis for most patients with genetic prion disease,” said Eric. “Only a minority of them.”

Although it doesn’t directly change Sonia’s prognosis, the new study may help develop drugs to treat prion disease. The study found that a few reduce the prion protein’s function among the benign mutations. Because carriers of these so-called “loss-of-function” mutations are apparently healthy, it suggests that developing drugs that work against the protein may be safe. Eric and Sonia are now working on developing molecules to do just that, and they can move in that direction more confidently.

Love and Science

In the context of prion disease, this study positively impacts the prognosis for a few hundred individuals worldwide while providing validation for a therapeutic strategy that may offer hope more broadly to patients and families affected by prion disease.

The researchers said that, more generally, the study also highlights the value of large reference datasets like 23andMe’s and Broad’s.

For this study, researchers used exome data from 60,000 people collected by the Broad Institute from a large international consortium and genotypic data from more than 530,000 23andMe customers who consented to research. Excitingly, as datasets of this size continue to grow, so will their power to expand and refine our understanding of human disease.

In the couple profile that appeared in the New Yorker in 2014, the writer quotes from an email he received from Sonia trying to describe her relationship with Eric.

“I thought when I married him that I could never love anyone more than I did that day. But I was wrong,” she said. “We are in a new dimension of partnership now, and I am more in love and, frankly, more in awe of him with every day we spend together. His brain is outstandingly powerful, and I see things I would never have known he was capable of in any other way. He was meant to do this work, and the world will be better for it.”

Love might not conquer all, but Eric and Sonia’s work points to what it can do when fueling the work of two brilliant minds.

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prion disease

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