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Contribution of Alzheimer’s disease risk genes in the maintenance of endolysosomal transport regulation

Alzheimer’s disease (AD) is the most common form of dementia of which the incidence increases with age. No cures are available yet, urging to explore new strategies for the identification of pathways that can be targeted therapeutically. Research in AD has been majorly driven by studying familial AD (FAD)‐associated mutations in the APP and PSEN genes, albeit they represent only a minor fraction of all cases. GWAS studies have identified ≈30 late‐onset AD (LOAD) susceptibility loci that, when functionally clustered, are directly or indirectly linked to cellular trafficking routes and functioning. These include genes linked to cholesterol metabolism (e.g. APOE4, ABCA7, INPP5D), endocytic transport regulation (e.g. BIN1, CD2AP, PICALM, SORL1) and lysosomal processes (e.g. GRN, PLD3). The genetic findings concur with the appearance of endolysosomal abnormalities at preclinical stages, before the appearance of senile plaques and tangles.