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Scientists, linking gene with serotonin and depression, offer insights to new treatments

ers analyzed tissue from a mouse model of depression as well as post-mortem tissue from depressed human patients, and found decreased levels of p11 protein in both cases. On the other hand, p11 levels increased in rats and mice that were treated with anti-depressant medications or electroconvulsive therapy.

To further test the connection, Svenningsson and his colleagues genetically engineered two strains of mice: one that produced more p11 than normal and another that produced no p11 at all. They found that mice that overexpress p11 were hyperactive and, in a test designed to identify depression in rodents, acted just like mice that were on anti-depressant medication. Mice that lacked p11, meanwhile, acted depressed and showed less responsivity to anti-depressant medications.

Taken together, the findings point to p11 as a new target for developing depression treatments.

"In addition to exploring ways to increase p11 in depressed patients, it may also be possible to develop peptide-based compounds that can mimic the action of p11 to achieve a new class of anti-depressant compounds," Svenningsson says.

In addition to Svenningsson and Greengard, the study's other authors are Ilan Rachleff and Marc Flajolet at Rockefeller; Karima Chergui and Xiaoqun Zhang at Karolinska; Malika El Yacoubi and Jean-Marie Vaugeois at the University of Rouen; and George G. Nomikos at Eli Lilly.


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Contact: Joseph Bonner
bonnerj@rockefeller.edu
212-327-8998
Rockefeller University
5-Jan-2006


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