P3‐327: Hsp90 inhibition rescues behavioral deficits and reduces tau phosphorylation in ps19 mice model for Alzheimer's disease (AD)

with neurotoxicity & ameliorates strain-specific tau-related phenotypes. Mice treated display no signs of toxicity; confirmed through pathology analysis following chronic administration. The inhibition of Hsp90 induced the expression of the pro-survival chaperone Hsp70, a chaperone also associated with tau degradation. Additionally, inhibiting the Hsp90-dependent protection of tau abrogated a terminal tau-driven phenotype thereby extending the lives of treated animals as compared to transgenic animals receiving vehicle or no treatment. Conclusions: Together, these findings demonstrate the potential for Hsp90 inhibition in the treatment of neurodegenerative diseases involving tau accumulation; namely, Alzheimer’s disease. Data accompanying this presentation which presents experimental behavioral changes and immunohistochemical analysis of neural tau burden can be seen on the poster presented by Inda, C. et al.