March 12, 2009
Michael J. Fox Foundation Joins Effort to Recruit 10,000 People with Parkinson's Disease to New Web-based PD Research Community
The Michael J. Fox Foundation for Parkinson’s Research, together with personal genetics company 23andMe of Mountain View, California, and The Parkinson’s Institute and Clinical Center of Sunnyvale, California, announced a call for 10,000 people with Parkinson’s disease to join an ambitious new research community. The goal of the community is to empower individuals with PD to proactively impact research in real time, potentially helping to speed early-stage scientific discoveries toward practical therapeutic relevance in treating Parkinson’s disease.
The 23andMe Parkinson’s Disease Community, conceived and led by 23andMe, is a novel attempt to leverage DNA technology, the Internet, and patient participation to enhance scientific understanding of Parkinson’s disease and the field’s ability to develop breakthrough treatments.
“Exploring the potential of a Web-based approach to patient engagement for research purposes is well-aligned with our Foundation’s mission,” said Katie Hood, CEO of The Michael J. Fox Foundation.
For the past year, the Foundation has been funding a partnership between 23andMe and the Parkinson’s Institute and Clinical Center to develop Web-based tools and surveys to gather information from a community of PD patients in a scientifically meaningful way. That project is still in development. In the interest of ensuring that the surveys can be put to immediate use once they are ready, 23andMe and the Parkinson’s Institute are now formally beginning the work of building the community.
To accelerate this community’s growth, through March 22, 23andMe is sponsoring up to 10,000 people with Parkinson’s to join the community for $25 instead of the usual $399. To be eligible for this discounted rate, individuals must have been diagnosed with Parkinson’s by a physician, be willing to provide a saliva sample for genetic analysis, and agree to participate in online surveys about their experience with Parkinson’s. Participants’ data will be kept anonymous, but will contribute to a larger pool of data about the PD community that will inform various Parkinson’s research efforts over time.
In addition, members will have full access to the 23andMe Personal Genome Service™, which includes detailed, personalized reports across many health conditions and traits, including PD. They will also have the opportunity to share their experiences directly with others in the 23andMe community who have Parkinson’s or who carry genetic markers placing them at increased risk for developing the disease.
More information on joining the community -- including information on how people with Parkinson's can obtain a discount code to participate in the limited-time reduced rate of $25 -- is available at http://michaeljfox.org/23andme.cfm
Related Article:
Google Co-Founder Backs Vast Parkinson's Study by Andrew Pollack
New York Times
Gene variation in the LRRK2 gene identifies a third of Parkinson’s Disease patients -- many more than the p.G2019S mutation.
While 2% of PD patients are known to carry a mutation in the LRRK2 gene called p.G2019S, fully a third have a specific genetic signature in LRRK2 unrelated to the mutation that is uncommon in the general population.
Researchers at the National Institute on Aging, University College London, and Matrix Genomics, Inc. have identified a concise genetic signature found among a third of Parkinson’s disease (PD) patients – but at very low frequency in the general population. The signature is found in the LRRK2 gene located on chromosome 12.
This study published in the Annals of Human Genetics
http://www3.interscience.wiley.com/journal/122399048/abstract
describes a combination of four gene variants found in a third of Parkinson’s cases, but infrequent in the population. Thus the presence or absence of this signature can be used as a genetic test for Parkinson’s disease. [Patent pending.]
Genetic testing using this approach is expected to identify a third of persons at very high risk. It will not identify other genetic factors or level of risk due to environmental exposures, such as pesticides, and lifestyle. Thus the absence of this risk signature does not guarantee low risk.
This finding helps us understand what causes PD and could lead to new and more effective avenues for prevention and treatment. The advance is expected to identify individuals at greatest risk for PD before symptoms arise, when therapies and lifestyle changes might be most effective in slowing disease progression.
In 1993, Dr. Corder the corresponding author on the paper was the lead author on the Science article that described how risk for Alzheimer’s disease multiplied according to the number of copies of the apolipoprotein E allele 4 inherited from parents. This finding has been replicated in hundreds of studies and remains the one established genetic risk factor for Alzheimer’s disease, and the prototype for investigating common gene variants for common disorders.
The LRRK2 text is available at the Matrix Genomics website: www.matrixgenomics.com.
Posted by: Elizabeth H. Corder, PhD | June 29, 2009 at 01:23 PM