Alzheimer’s disease (AD) is the leading cause of dementia worldwide, with no cure currently available. AD pathogenesis is primarily driven by cerebral accumulation of β-amyloid (Aβ), a small peptide and proteolytic cleavage product of amyloid-β precursor protein (APP). Elucidating molecular mechanisms that change Aβ levels and APP processing could provide new insights for understanding disease etiology; and development of interventions that attenuate amyloid pathology may provide useful therapeutics for AD.