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Saturday June 30 6:46 AM ET Gene Research Suggests How Parkinson's Might Arise By Amy Norton NEW YORK (Reuters Health) - Research into the genetic roots of inherited forms of Parkinson's disease (news - web sites) may have opened the door to understanding how all forms of the degenerative disorder arise. An international team of scientists has found that two proteins linked to inherited Parkinson's interact in healthy brains--suggesting that a misstep in this interaction may be involved in all cases of Parkinson's. If future research bears out this concept, it may be possible to design a drug that specifically targets the protein-gone-wrong, study co-author Dr. Michael G. Schlossmacher of Harvard Medical School (news - web sites) in Boston, Massachusetts, said in an interview. He and his colleagues report their findings in the June 28th issue of Sciencexpress, the online edition of the journal Science. Not long ago, researchers believed Parkinson's disease had no genetic component. But in recent years, scientists have identified gene mutations linked to inherited Parkinson's--rare forms of the disease that typically strike relatively young people. Parkinson's usually affects people older than 50, causing tremors, muscle rigidity, and balance and coordination problems that worsen over time. All cases of Parkinson's are marked by a loss of certain brain cells that help control movement. All patients also have an accumulation of a protein called alpha-synuclein in their brains, according to Schlossmacher. In fact, scientists recently discovered that a mutation in the gene for alpha-synuclein is responsible for one of the inherited forms of the disease. Mutations in another gene, called parkin, have been implicated in causing a second inherited type of Parkinson's To see what role the parkin and alpha-synuclein proteins might play in common forms of Parkinson's, Schlossmacher and his colleagues examined both healthy brain tissue and tissue from patients with Parkinson's due to a parkin mutation. They found that parkin and alpha-synuclein interact in healthy brains, with parkin helping to clear alpha-synuclein from cells. In brains affected by the inherited form of Parkinson's, however, parkin could not do its job, causing alpha-synuclein to accumulate. Because parkin and alpha-synuclein have a healthy working relationship in normal brains, Schlossmacher and his colleagues hypothesize that an abnormality in this interaction may be at the root of Parkinson's. Even though most patients do not have an overt mutation in these genes, Schlossmacher explained, they may have a ``subtle abnormal tuning'' in the interaction between the two proteins that allows alpha-synuclein to accumulate in the brain. If alpha-synuclein build-up is the trigger for the loss of nerve cells in Parkinson's, it may be possible to design drugs that bring down levels of alpha-synuclein, Schlossmacher said. However, he stressed, this scenario remains about 10 years away. This study, he said, is a ``first and significant step'' in understanding how Parkinson's disease begins. SOURCE: Sciencexpress 2001;10.1126. http://dailynews.yahoo.com/h/nm/20010630/hl/parkinsons_1.html * * * ---------------------------------------------------------------------- To sign-off Parkinsn send a message to: mailto:[log in to unmask] In the body of the message put: signoff parkinsn