Chunk #95 — Results and discussion — Analysis of Akt/mTOR phosphoprotein pathway throughout the brain after chronic alcohol: Decreased expression of multiple mTOR/Akt phosphoproteins in 3xTg-AD alcohol-exposed mice (1-month post alcohol) — Entorhinal cortex
The entorhinal cortex is sensitive to early AD pathology and this is reflected in both the brain and behavior. It is relevant in AD pathology in part because of a major pathway projecting from the AMY to the entorhinal (primarily lateral) as well as a substantial pathway projecting from the entorhinal cortex to the HPC. However, to date, the only study that has considered the role of the mTOR pathway in the AD pathology of the entorhinal cortex did so by pharmacologically inhibiting mTOR via chronic systemic treatment with rapamycin (Siman, Cocca, & Dong, 2015). This group observed a decrease in Tau-induced neuronal loss in the LEC, but not total Tau or mRNA levels. Our results suggest notable dysfunction of both the LEC and MED mTOR/Akt phosphoproteins after chronic alcohol consumption. In the LEC, alcohol drinking significantly decreased IGF1R [t(8) = 1.905, P = 0.047], IR [t(8) = 2.211, P = 0.029], and PTEN [t(8) = 1.976, P = 0.042]; while in the MEC, GSK3α [t(7) = 2.590, P = 0.018], IGF1R [t(7) = 2.949, P = 0.011], IRS1 [t(7)
