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Originally published October 14 2005

Yale researchers uncover gene that may be linked to Tourette's Syndrome

by Mike Adams, the Health Ranger, NaturalNews Editor

Science has published a report authored by Matthew State, Harris Assistant Professor in the Yale Child Study Center, that identifies a gene known as SLITRK1, which apparently contributes to some cases of TS.



Researchers At Yale Identify A Genetic Link To Tourette's Syndrome New Haven, Conn. --- In what may be a major milestone in Tourette's Syndrome (TS) research, scientists at Yale School of Medicine and their colleagues have identified a gene called SLITRK1 that appears to contribute to some cases of TS, according to a report in the October 14 issue of Science. "We now have rare mutations, expression and functional data, all supporting a role for this gene in Tourette's Syndrome," said senior author Matthew State, M.D., Harris Assistant Professor in the Yale Child Study Center and in the Department of Genetics at Yale. TS is a relatively common neurological disorder characterized by tics---involuntary, rapid, sudden movements or vocalizations that occur repeatedly in the same way. State said TS patients swearing uncontrollably is actually uncommon, with only a small percentage of TS patients ever having this symptom. For years, many researchers sought a single, abnormal gene for TS. While many researchers looked for genetic similarities among large groups of TS patients, State and his team took the opposite approach pioneered by co-author and Yale's Chair of Genetics, Richard Lifton, M.D., of searching for unusual patients with TS. With help from the Tourette Syndrome Association, they found such a case in which a child had TS and carried a chromosomal abnormality. Working with Yale neurobiologists and co-authors Nenad Sestan and Angeliki Louvi, the team used molecular methods to identify differences in that child's DNA. The team found an abnormal DNA sequence in one family and the identical, very rare change in the DNA sequence in two unrelated people. This second finding was in a non-coding region of the gene that does not directly make protein.


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