FRIDAY, Jan. 18 (HealthDay News) -- Predicting brain disorders such as Parkinson's disease and amyotrophic lateral sclerosis (ALS) may be possible by identifying certain DNA fingerprints, a recent Mayo Clinic study suggests.
The researchers analyzed the genetic data of people with ALS (also known as Lou Gehrig's disease) and Parkinson's, and those without neurological disorders. They pinpointed several gene variations that predicted who was at higher risk for developing the disorders, according to the study published online in PLoS One.
The variations were found by studying the axon guidance pathway, a complex collection of chemical signals that wire the brain during fetal development, and maintain and repair brain circuits throughout a person's life.
Researchers found many variations within pathway genes common to ALS and Parkinson's. However, they also identified several that collectively indicate people at high risk (2,000 times greater than the general population) for ALS. And they pinpointed several gene variations that collectively predicted people at high risk (nearly 400 times greater than the general population) for Parkinson's disease.
"In persons at high risk, we may be able to prevent the diseases or slow or halt their progression by developing drugs that target the same disease pathways. For ALS and Parkinson's disease, our study is a major step in these directions," principal investigator and Mayo Clinic neurologist Dr. Demetrius Maraganore said in a prepared statement.
ALS is a progressive neurodegenerative disease that leads to loss of muscle control and use, and eventually death. As many as 30,000 Americans have the disease at any given time, according to the ALS Association. Parkinson's disease, a brain disorder that affects 1.5 million Americans, causes tremors, slowness of movement, and body stiffness, according to the National Parkinson Foundation. No cure exists for either disease.
More information
The Muscular Dystrophy Association has more about ALS.
-- Robert Preidt
SOURCE: Mayo Clinic, news release, Jan. 15, 2008
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