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Reversal of aging by NFκB blockade

Adam S. Adler, Tiara L.A. Kawahara, Eran Segal and Howard Y. Chang

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Genetic studies in model organisms such as yeast, worms, flies, and mice leading to lifespan extension suggest that longevity is subject to regulation. In addition, various system-wide interventions in old animals can reverse features of aging. To better understand these processes, much effort has been put into the study of aging on a molecular level. In particular, genome-wide microarray analysis of differently aged individual organisms or tissues has been used to track the global expression changes that occur during normal aging. Although these studies consistently implicate specific pathways in aging processes, there is little conservation between the individual genes that change. To circumvent this problem, we have recently developed a novel computational approach to discover transcription factors that may be responsible for driving global expression changes with age. We identified the transcription factor NfκB as a candidate activator of aging-related transcriptional changes in multiple human and mouse tissues. Genetic blockade of NFκB in the skin of chronologically aged mice reversed the global gene expression program and tissue characteristics to those of young mice, demonstrating for the first time that disruption of a single gene is sufficient to reverse features of aging, at least for the short-term.

Authors

Adam S. Adler

Stanford University School of Medicine; Stanford, CA

Tiara L.A. Kawahara

Stanford University School of Medicine; Stanford, CA

Eran Segal

Weizmann Institute of Science; Rehovot, Israel

Howard Y. Chang

Stanford University School of Medicine; Stanford, CA

Purchase article for $19

Subscribe to this journal for $129/year