While studying these side effects, which are called dyskinesia, Kovoor discovered that RGS9 2 also plays a role in regulating body weight. Kovoor and his collaborators found that humans with a gene variation that could reduce RGS9 2 levels had a significantly higher body mass index.
Because RGS9-2 is normally expressed in the brain's striatum, a section of the brain involved in both motor control and reward responses, Kovoor and his fellow researchers thought that the weight gain could be a result of an increased reward response triggered during eating.
"Our research shows that the striatum, through RGS9-2, has a role in regulating body weight that is independent of the motivation, movement and reward responses," Kovoor said. "We have identified a new gene that likely regulates weight gain through metabolism."
Surprised by the discovery, Kovoor said he and his team have been studying RGS9-2 and its role in the movement side effects of drug therapy for Parkinson's disease and schizophrenia for almost a decade.
"We treated RGS9-2 knockout mice (those without the RGS9-2 gene) with anti-psychotic drugs or with L-DOPA, a drug used to treat Parkinson's disease, and the mice all rapidly developed dyskinetic movement disorders when being treated.
In fact, prompted by Kovoor's discovery, one of his collaborators, Stephen Gold, and his colleagues at the University of Texas, were able to show that gene therapy with RGS9-2 could suppress drug-induced dyskinesias in monkeys.
"Separately, we were looking to see if we could predict the risk susceptibility for these (movement) disorders by searching for variations in the RGS9-2 gene in humans."
Kovoor and his fellow researchers at the University of California in San Francisco also monitored the body mass index of patients in their study. "We noticed that study subjects with a variation in the RGS9-2 gene, which could weaken expression of the gene, had a higher body mass index."
MEDICA.de; Source: University of Rhode Island