In his new personal blog, started yesterday, famed Google founder and multibillionaire Sergey Brin delves immediately into a deeply personal subject: his genetic risk for Parkinson’s disease. Brin, whose mother suffers from Parkinson’s, learned that he carries a mutation linked to increased risk of the disease after being screened by 23andMe, a personal-genomics startup cofounded by his wife, Anne Wojcicki.
23andMe’s brand of direct-to-consumer testing has garnered criticism from the genomics community for going on the market before scientists have had a chance to assess whether such tests can actually help, or would possibly hinder, an individual’s health. (If someone finds out that she is at greater risk for type 2 diabetes, for example, she may adopt a fatalistic attitude, eating junk food and not exercising.) Critics are also concerned that the general public won’t be able to understand the subtleties of the test: 23andMe’s service identifies genetic variations that may increase an individual’s risk of disease, but that does not mean that the carrier will ever get it. (A review in our current issue argues against this point of view.)
While Brin doesn’t discuss why he decided to go public with his results, perhaps he wants to use his role as an Internet celebrity and, in some sense, experimental test subject to better educate the public. His post nicely outlines the limitations of personal-genomics testing and discusses what an individual can do once he learns his own risks, even for a disease like Parkinson’s, with few proven preventative interventions. Better public understanding of these issues is going to be crucial as personal genomics makes its way into medical care, be it through companies like 23andMe or other venues. (Cynical readers, of course, might see an alternative motive: an attempt to drum up interest in his wife’s company’s service, in which Google has invested.)
From Brin’s post:
…The exact implications of this are not entirely clear. Early studies tend to have small samples with various selection biases. Nonetheless it is clear that I have a markedly higher chance of developing Parkinson’s in my lifetime than the average person. In fact, it is somewhere between 20% to 80% depending on the study and how you measure. At the same time, research into LRRK2 looks intriguing (both for LRRK2 carriers and potentially for others).
This leaves me in a rather unique position. I know early in my life something I am substantially predisposed to. I now have the opportunity to adjust my life to reduce those odds (e.g. there is evidence that exercise may be protective against Parkinson’s). I also have the opportunity to perform and support research into this disease long before it may affect me. And, regardless of my own health it can help my family members as well as others.
I feel fortunate to be in this position. Until the fountain of youth is discovered, all of us will have some conditions in our old age only we don’t know what they will be. I have a better guess than almost anyone else for what ills may be mine – and I have decades to prepare for it.
In an article that I wrote for Tech Review two years ago on the study linking this genetic variation to Parkinson’s disease in Ashkenazi Jews, scientists speculated on future clinical testing. (Brin is of Jewish descent.)
While gene testing for diseases that have no known cure, such as Parkinson’s, is controversial, Laurie J. Ozelius, a molecular geneticist at Albert Einstein College of Medicine of Yeshiva University in the Bronx, who was involved in the research, says testing still could have some advantages. “People who come to the doctor [with symptoms of Parkinson’s] already have a lot of degeneration. Now we can look at [earlier] stages of the disease,” she says. “If we find treatments that slow the disease, it’s better to identify a gene carrier so we can start the treatment earlier.”
Susan B. Bressman, senior investigator of the report and a neurologist at Einstein, says that having a group with a known risk for Parkinson’s will aid in future studies of the disorder. Because not everyone with the mutation will go on to develop the disease, scientists can try to identify the genetic or environmental factors that put some people at greater risk. Scientists could also test potential neuroprotective drugs in this group much more efficiently than in a general population.
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