National Institutes of Health [R01AG038710, R01AG021173, R01AG044420, R01NS046673]; Alzheimer's Association; National Natural Science Foundation of China [81225008, 81000540, 81161120496, 91332112, 91332114]; Fundamental Research Funds for the Central Universities of China; Fok Ying Tung Education FoundationThe beta-amyloid (A beta) peptide has been postulated to be a key determinant in the pathogenesis of Alzheimer's disease (AD). A beta is produced through sequential cleavage of the beta-amyloid precursor protein (APP) by beta-and gamma-secretases. APP and relevant secretases are transmembrane proteins and traffic through the secretory pathway in a highly regulated fashion. Perturbation of their intracellular trafficking may affect dynamic interactions among these proteins, thus altering A beta generation and accelerating disease pathogenesis. Herein, we review recent progress elucidating the regulation of intracellular trafficking of these essential protein components in AD
