Sci. Signal., 8 November 2011
Cell Biology Exercise for Life
Stella M. Hurtley
Science, AAAS, Cambridge CB2 1LQ, UK
An unresolved issue in the field of neurodegenerative diseases is whether exercise would have long-lasting beneficial effects or whether it would have deleterious long-term consequences by increasing the metabolic demands on already susceptible neuronal populations. Fryer et al. (see the Perspective by Gitler) now show that exercise significantly extended the life span of a mouse model for the polyglutamine neurodegenerative disorder spinocerebellar ataxia type 1 (SCA1). Exercise up-regulated epidermal growth factor, which caused down-regulation of Capicua (Cic), a transcriptional repressor that interacts with Ataxin-1 in vivo. In Cic mutant mice, all SCA1 phenotypes were rescued, including premature lethality, by reducing the level of Cic by 50%.
J. D. Fryer, P. Yu, H. Kang, C. Mandel-Brehm, A. N. Carter, J. Crespo-Barreto, Y. Gao, A. Flora, C. Shaw, H. T. Orr, H. Y. Zoghbi, Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua. Science 334, 690–693 (2011). [Abstract] [Full Text]
Citation: S. M. Hurtley, Exercise for Life. Sci. Signal. 4, ec314 (2011).
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