Figure 1: Theories regarding the pathogenesis of AD. (A) Amyloid-β plaque theory. APP is degraded into Aβ monomers, which then assemble into Aβ oligomers and ultimately pathological Aβ plaques. (B) Tau NFT theory. Abnormal post-translational modification of Tau (especially hyperphosphorylation) promotes Tau-Tau interactions, leading to the sequential formation of tangles, PHFs, and NFTs. (C) Neuroinflammation theory. Quiescent immune cells in the CNS (mainly microglia and astrocytes) can be activated by toxic Aβ aggregates and then secrete a large number of proinflammatory cytokines, leading to chronic inflammation. (D) Oxidative stress theory. Certain pathological stimuli (e.g., Aβ plaques and NFTs) can disrupt metal homeostasis and mitochondrial dysfunction, both of which increase ROS generation and cause neurodegeneration due to oxidative injury. These four mechanisms may work independently or interactively, eventually resulting in AD pathology, including cerebral cortical shrinkage, ventricular enlargement, and hippocampal atrophy. AD: Alzheimer’s disease; APP: amyloid precursor protein; Aβ: beta-amyloid peptide; CNS: central nervous system; NFT: neurofibrillary tangle; PHF: paired helical filament; ROS: reactive oxygen species.