线粒体在阿尔茨海默病中的分子机制及治疗策略研究进展OA

Alzheimer's disease(AD),the most prevalent neu-rodegenerative disorder among the elderly,is characterized by progressive cognitive decline.Traditional AD research has pri-marily focused on amyloid-β-protein(Aβ)plaques and Tau neurofibrillary tangles.Recent studies indicate that mitochon-drial dysfunction plays a central role in the pathogenesis of AD.As the energy-supplying organelles of neurons,mitochondrial dysfunction leads to reduced ATP production,increased oxida-tive stress,and a cascade of cellular consequences that impair neuronal function,ultimately triggering neuronal death and AD symptoms.Mitochondrial dysfunction is closely linked to hall-mark AD features such as Aβ plaque deposition and hyperphos-phorylated Tau,forming a vicious cycle that accelerates neuro-degeneration.Mitochondrial dysfunction,including mitophagy,mitofission and mitofusion,and mitochondrial injury,disrupts mitochondrial morphology maintenance and quality control,po-tentially serving as a key factor in AD neuropathology.This re-view examines the interaction mechanisms between mitochon-dria and AD,as well as drugs targeting mitochondria for AD treatment,aiming to provide new paradigms for developing pre-cision intervention strategies against AD.