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Exercise, as a multi\u2010target therapeutic modality, has been shown to reverse multiple facets of AD\u2010related neuropathology through diverse mechanisms. In this systematic review, we synthesize evidence on the effects of voluntary running, structured swimming, and modulation of the gut microbiota in transgenic murine models of AD. Exercise was found to ameliorate AD pathology by modulating amyloid precursor protein (APP) processing and \u03b2\u2010amyloid (A\u03b2) production\/clearance, restoring mitochondrial integrity and function, attenuating neuroinflammatory responses, enhancing synaptic plasticity, and upregulating neurotrophic factors. Moreover, exercise reshapes the intestinal microbiome and thereby modulates the gut\u2013brain axis, further promoting neuroimmune homeostasis and cognitive resilience. Through RNA sequencing data analysis, key genes such as Tlr4, Cdc42, and F13a1 were identified, which may play significant roles in neuroimmune regulation and cognitive protection. By integrating multi\u2010omics evidence, we propose a coordinated \u201cexercise\u2013microbiota\u2013brain\u201d mechanistic framework that offers theoretical support for personalized, exercise\u2010based therapeutic strategies and translational applications in AD. 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