fig2

Figure 2. Pathological cascade of AD. Aberrant proteolytic cleavage of APP generates Aβ peptides with strong aggregation propensity. These peptides accumulate extracellularly to form insoluble Aβ plaques, which trigger microglial activation and astrocytic reactivity. Activated glial cells release proinflammatory cytokines, creating a neurotoxic microenvironment. Meanwhile, intracellular tau undergoes pathological hyperphosphorylation, leading to NFT formation. The synergy of Aβ-driven neuroinflammation, tau pathology, and glial activation ultimately disrupts BBB integrity and drives progressive neurodegeneration in the brain parenchyma. [Created in BioRender. Y, S. (2025) https://BioRender.com/4lv920b]. AD: Alzheimer’s disease; APP: amyloid precursor protein; Aβ: amyloid-β; NFT: neurofibrillary tangle; BBB: blood-brain barrier.