Pyroptosis: a potential target and research progress of exercise in ameliorating Alzheimer's disease pathology

Alzheimer's disease (AD), a debilitating neurodegenerative disorder that severely threatens elderly health, is clinically manifested as cognitive decline and driven by core pathological hallmarks including amyloid-beta (Aβ) deposition, tau hyperphosphorylation, and chronic neuroinflammation. Recent studies have indicated that its pathophysiological process is closely associated with pyroptosis, and excessive activation of pyroptosis drives a vicious cycle of amplified inflammation and neuronal injury. Although accumulating evidence suggests that exercise serves as an effective non-pharmacological intervention to suppress pyroptosis and alleviate AD, the intrinsic interactive mechanisms among exercise, pyroptosis and the pathological progression of AD remain incompletely elucidated. Therefore, this review systematically summarizes the functional mechanisms of pyroptosis in the pathological progression of AD and discusses the potential neuroprotective effects of exercise intervention. It further focuses on analyzing the specific mechanisms by which exercise inhibits pyroptosis via regulating the NLRP3 inflammasome pathway, aiming to identify novel targets for the prevention and treatment of AD and provide a theoretical basis for formulating scientific exercise intervention strategies.