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dc.contributor.authorUrban, Michael Joseph
dc.contributor.authorDobrowsky, Rick T.
dc.contributor.authorBlagg, Brian S. J.
dc.date.accessioned2017-04-17T20:28:28Z
dc.date.available2017-04-17T20:28:28Z
dc.date.issued2011-12-13
dc.identifier.citationUrban, Michael J., Rick T. Dobrowsky, and Brian S.J. Blagg. “Heat Shock Response and Insulin-Associated Neurodegeneration.” Trends in Pharmacological Sciences 33.3 (2012): 129–137.en_US
dc.identifier.urihttp://hdl.handle.net/1808/23716
dc.description.abstractDysfunctional insulin and insulin-like growth factor-I (IGF-I) signaling contributes to the pathological progression of diabetes, diabetic peripheral neuropathy (DPN), Alzheimer's (AD), Parkinson's (PD) and Huntington's diseases (HD). Despite their prevalence, there are limited therapeutic options available for the treatment of these neurodegenerative disorders. Therefore, establishing a link between insulin/IGF-I and the pathoetiology of these diseases may provide alternative approaches toward their management. Many of the heat shock proteins (Hsps) are well-known molecular chaperones that solubilize and clear damaged proteins and protein aggregates. Recent studies suggest that modulating Hsps may represent a promising therapeutic avenue for improving insulin and IGF-I signaling. Pharmacological induction of the heat shock response (HSR) may intersect with insulin/IGF-I signaling to improve aspects of neurodegenerative phenotypes. Herein, we review the intersection between Hsps and the insulin/IGF systems under normal and pathological conditions. The discussion will emphasize the potential of non-toxic HSR inducers as viable therapeutic agents.en_US
dc.publisherElsevieren_US
dc.rightsCopyright Elsevieren_US
dc.titleHeat shock response and insulin-associated neurodegenerationen_US
dc.typeArticleen_US
kusw.kuauthorBlagg, Brian S. J.
kusw.kudepartmentMedicinal Chemistryen_US
dc.identifier.doi10.1016/j.tips.2011.11.001en_US
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.rights.accessrightsopenAccess


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