Chunk #78 — Results and discussion — NIA-AA biomarker analysis in specific brain regions of 3xTg-AD mice (1-month post alcohol) — Lateral entorhinal cortex (LEC)
Alcohol intake significantly increased Aβ (42/40) ratio [t(7) = 4.1, P = 0.004] and total Tau protein [t(7) = 3.57, P = 0.009] as compared to saccharin control (Fig. 6A). This pathology profile is consistent with Alzheimer’s disease and concomitant non-Alzheimer’s pathologic change (e.g., A + T − (N)+) because elevated total Tau, in the absence of pTau, may reflect general neuropathology (Table 2). Since the initial (mild) stage of AD is characterized by Aβ and Tau pathology in the LEC (Braak & Braak, 1998; Khan et al., 2014; Palmer et al., 2011), these results support the interpretation that alcohol drinking enhanced the onset of AD-like neural pathology in 3xTg-AD mice.
