The Mitochondria is the Source of Hepatic Amyloid Precursor Protein and Peripheral Amyloid Beta: Implications of Alcohol‐induced Liver Steatosis in Alzheimer's Disease

Differential expression of APP across mitochondrial subpopulations suggests that hepatic mitochondria may be a source of peripheral aB and affect specific mitochondrial processes in the GM and ERM. Increased expression of APP in the pericentral region of AD mice correlates to the same site affected in alcohol-induced liver damage and may assist in identifying potential pathways involved in AD progression due to alcohol-induced liver impairment. Future studies modulating hepatic APP in vivo will provide future insights on the contribution of hepatic aB on AD pathogenesis.