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Characterized by progressive cognitive decline\u2014including deficits in memory, executive functions, and language, alongside behavioral disturbances\u2014AD arises from complex pathophysiological mechanisms. These include neurotransmitter imbalances, cholinergic deficits, amyloid-beta (A\u03b2) toxicity, tau protein hyperphosphorylation, oxidative stress, synaptic dysfunction, and neuroinflammatory processes. Growing evidence highlights the protective role of microglia in AD pathology through their immune functions, phagocytic clearance of A\u03b2 proteins, and trophic support to promote tissue repair and maintain cerebral homeostasis, as alterations in their response to A\u03b2 are linked to an increased risk of AD. However, disruptions in homeostasis or tissue alterations may trigger microglial activation, leading to detrimental effects such as increased inflammatory activity, impaired microglial-mediated clearance, synapse loss, and neuronal damage. 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