Chunk #82 — Results and discussion — NIA-AA biomarker analysis in specific brain regions of 3xTg-AD mice (1-month post alcohol) — Biomarker conclusions
First, based on evidence that 6–8-month-old 3xTg-AD mice exhibit AD-like pathology expressed as increased Aβ in the HPC, cortex, and AMY (Oddo, Caccamo, Shepherd, et al., 2003), these data suggest that alcohol increased the magnitude of AD-like pathology in the LEC and PFC during the initial cortical stages (e.g., Fig. 2). Second, 3xTg-AD mice are known to exhibit Tau pathology at 12–15 months; thus, the appearance of elevated total Tau in LEC, mPFC and AMY at 8months of age suggests that alcohol drinking promoted rapid onset of pathology in these brain regions. Third, it is important to note that these data were obtained 1month after alcohol use suggesting the presence of a long-term negative impact on AD-like pathology. Moreover, by focusing on biomarkers within the NIA-AA Research Framework, these findings integrate with the broader field of age-related neurodegeneration and suggest that alcohol use is a risk factor for AD-like pathology in vulnerable individuals. Increased knowledge of specific pathologies associated with alcohol use in AD has the potential to aid diagnosis and treatment.
