After the gene was delivered to the animals' p11-inhibited nucleus accumbens regions, the mice stopped displaying depressive behaviors, the researchers reported.
What's more, autopsies conducted on human patients who had been diagnosed with severe depression further revealed that the same region in their brains had significantly lower amounts of the p11 gene than typically found in patients with no signs of depression, the study noted.
"Together, these studies provide strong evidence that maintaining adequate levels of this particular protein, p11, in this pleasure-reward area of the brain may be central to preventing or treating depression," Kaplitt concluded.
However, "patients should not get their hopes up that this is going to turn around the treatment of depression anytime soon," according to Dr. Bernard Carroll, scientific director of the Pacific Behavioral Research Foundation in Carmel, Calif., and a former chairman of the U.S. Food and Drug Administration's advisory committee for psychotropic drugs.
"The laboratory findings are interesting, but the translational step to anything that would benefit a patient is very removed at this point," he noted. "Although the basic neurobiology that is being studied here is well known, depression is a human disorder and animal models do not faithfully reproduce the full syndrome. So while I'm not knocking the science, what I'm knocking is the rush to speculate about how far this will take us."
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