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Anson Pierce, Natalia Podlutskaya, Jonathan J. Halloran, Stacy A. Hussong, Pei-Yi Lin, Raquel Burbank, Matthew J. Hart and Veronica Galvan Over-expression of heat shock factor 1 phenocopies the effect of chronic inhibition of TOR by rapamycin and is sufficient to ameliorate Alzheimer's-like deficits in mice modeling the disease Journal of Neurochemistry 124

Version of Record online: 26 DEC 2012 | DOI: 10.1111/jnc.12080

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Chronic inhibition of TOR or overexpression of HSF1, the master regulator of the heat shock response reduce amyloid, upregulate chaperones, and improve cognitive function in mice modeling Alzheimer's disease (AD). We propose that a mechanism by which chronic inhibition of TOR alleviates cognitive deficits involves preventing a decline in proteostasis that critically enables pathogenic processes of AD in aged brains.

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