Alzheimer's disease (AD), commonly observed in the elderly, manifests clinically with symptoms such as memory decline and neuropsychiatric abnormalities. The pathogenesis of AD remains unclear to date, as the various existing hypotheses fail to fully account for all the disease characteristics of AD. Microglia, specialized macrophages in brain tissue, monitor the health of surrounding neurons and glial cells, exhibiting both neuroprotective and neurotoxic effects. Recent in-depth research on AD has revealed that microglia participate in the pathogenesis of AD through the triggering receptor expressed on myeloid cells 2 (TREM2). Loss of TREM2 function exacerbates the progression of AD. This article reviews the role of TREM2 and its mutants in mediating microglial functional alterations during the occurrence and development of AD.