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P2‐033: Jnk: Bridging the insulin signaling and vglut1 in Alzheimer's disease
Author(s) -
Perdigon Manuel Rodriguez,
Zubiaurre Maite Solas,
Ramírez Gil María Javier
Publication year - 2015
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2015.06.569
Subject(s) - morris water navigation task , insulin receptor , medicine , endocrinology , insulin , glutamate receptor , insulin degrading enzyme , hippocampus , chemistry , glutamatergic , receptor , insulin resistance
(active form), while had no effect on the level of Tyrosine-307phosphorylated PP-2A. Unexpectedly, 5-HT1A agonist 8-OHDPAT did not decrease forskolin-induced tau hyperphophorylation. Conclusions:Escitalopram could protect forskolin-induced tau hyperphosphorylation at multiple AD-related sites, and the mechanism involves inactivation of GSK-3b. Our findings suggest that escitalopram could be a promising therapeutic target for AD-like tau hyperphosphorylation, this may support a potential effective role of antidepressants, at least of the SSRI class, in the prevention of dementia associated with depression in patients.