Alcoholism and Alzheimer’s disease are both neuroinflammatory and neurodegenerative disorders and as such, may share an overlapping etiology. The data show that indeed, the neuropathological changes that are associated with both disorders can be linked to mechanisms related to AB, Tau and the mToR pathway. The relevance of our alcohol proteomic networks to AD indicate that there may be important systems that could be useful early biomarkers (CRMP, HSK, AMPH, GSK) for identifying at-risk populations that could be then targeted with medications (tianeptine, lacosamide, tideglusib) with prophylactic treatment to prevent or minimize the development of AD. Given the strength of these associations, further research in both clinical and preclinical populations to test these hypotheses is warranted. Together, these data strongly suggest that some (or all) of these molecular mechanisms may be dysregulated by moderate alcohol use and that this may increase risk for developing and or exacerbating AD in susceptible populations.
