You are currently viewing the abstract.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Abstract
In this issue of Science Translational Medicine, Alexander and colleagues describe coherent evidence drawn from humans and from modeled animals that supports a brain region–specific gene therapy for depression: adeno-associated virus (AAV)–mediated transfer of the gene encoding p11 to the nucleus accumbens (NAcc). The investigators found that focal NAcc knockdown of p11 expression in mice resulted in behavioral deficits related to depression and that AAV-mediated p11 gene transfer to the NAcc rescued the depression-related behavioral deficits of mice in which endogenous p11 had been genetically knocked out. They also found that p11 levels were lower in the NAcc of patients with depression than in the NAcc of matched controls. Taken together, the data suggest that gene therapies aimed at enhancing p11 in the NAcc may represent promising new approaches for treating depression; however, a large number of clinical and regulatory issues must be overcome before such therapies can be implemented.
Footnotes
-
Citation: G. Chen, R. Twyman, H. K. Manji, p11 and gene therapy for severe psychiatric disorders: A practical goal? Sci. Transl. Med. 2, 54ps51 (2010).
- Copyright © 2010, American Association for the Advancement of Science