The article discusses the critical role of the mitochondrial contact site and cristae organizing system (MICOS) complex in the pathogenesis of Alzheimer's disease (AD). It highlights how MICOS abnormalities, including subunit dysfunction and interactions with disease-associated proteins, to hallmark AD pathologies such as amyloid-β accumulation, neurofibrillary tangle formation, and neuronal apoptosis. The article suggests that targeting MICOS subunits with pharmacological interventions may provide novel therapeutic insights for AD treatment.