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P1‐099: CIG SUPPRESSES TAU PATHOLOGY IN A MOUSE MODEL OF TAUOPATHY THROUGH REGULATING THE ACTIVITY OF PP2A
Author(s) -
Ma Denglei
Publication year - 2019
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.2019.06.654
Subject(s) - tauopathy , protein phosphatase 2 , phosphorylation , hyperphosphorylation , phosphatase , western blot , microbiology and biotechnology , tau protein , biology , protein tyrosine phosphatase , neuroscience , neurodegeneration , chemistry , biochemistry , alzheimer's disease , medicine , disease , gene
with DHAwas determined according to the median-effect principle and classical isobologram equation of Chou-Talay (Chou, 2006). Calculations were performed using CompuSyn software (v1.0). Dose-response curves were plotted for each compound to calculate their respective doses with 50% effect (ED50) in determining synergism. Synergismwas confirmed by combination index (CI) calculations < 1. Results: Out of the nine combinations used, luteolin at 5mMand DHA at 10mMwas determined as slightly synergistic with a CI value of 0.83 and all other combinations had antagonistic effects. Conclusions: Further studies in other cell lines are required to determine the optimal concentrations and combinations of luteolin and DHA to exert a synergistic effect in neutralizing Ab1-42 -induced toxicity.
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