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Originally published February 13 2006

Neuroscientist identifies protein that fights depression

by Mike Adams, the Health Ranger, NaturalNews Editor

Paul Greengard, a neuroscientist at Rockefeller University in New York City, led a study that found a protein called p11 helps stave off depression.



The protein, called p11, appears to help regulate signaling of the brain chemical serotonin. A target of the antidepressants called selective serotonin reuptake inhibitors (SSRIs), which include Prozac, serotonin has been linked to depression and anxiety disorders, the study noted. The experiments with mice revealed how p11 works with the serotonin receptor 5-HT1B, which has also been associated with obsessive-compulsive disorder, drug addiction, anxiety and aggression, as well as depression. The findings appear in the Jan. 6 issue of Science. "P11 can be viewed as a protein that links the pathophysiology of depression with the serotonin system," said lead study author Per Svenningsson, from the department of physiology and pharmacology at the Karolinska Institute, in Stockholm, Sweden. "The released serotonin acts on 14 serotonin receptors, some of which mediate therapeutic actions and some of which mediate side effects," he added. The researchers studied one specific serotonin receptor, the 5-HT1B receptor, and found that it interacts with p11. The protein is depleted in tissue in so-called "helpless" mice, which exhibit behaviors similar to depressed humans. "Mice that over-express p11 are hyperactive, and act as if they are on antidepressant medication," Svenningsson said. Conversely, mice that have no p11 "act as they are somewhat depressed and show less responsivity towards antidepressant medications," he added. While there's no immediate clinical application for this finding, Svenningsson said "this study emphasizes that 5-HT1B receptor, with its interaction with p11, may be linked to depression." One expert agrees that p11 might become a target for antidepressants in the future. "Whilst p11 is a potential source of new therapies, unfortunately at the moment we do not know enough about p11 to target it selectively with drugs," said Trevor Sharp, a reader in pharmacology at the University of Oxford, Great Britain, and author of an accompanying perspective article in the journal.


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