Microglial cells—the brain's resident immune sentinels—appear to drive Alzheimer's disease through their dysregulated cellular cleanup functions, according to emerging mechanistic evidence. These cells normally engulf and clear harmful protein aggregates, but aging disrupts this protective process while simultaneously triggering destructive phagocytosis of healthy synapses and neurons. The analysis connects over 25 known genetic risk factors for Alzheimer's, including APOE, TREM2, and CD33, to microglial phagocytic pathways. This framework offers a unifying explanation for why anti-amyloid antibody treatments—the only approved disease-modifying therapies—show modest efficacy by enhancing microglial clearance of amyloid plaques. The dual nature of microglial phagocytosis creates a therapeutic paradox: enhancing clearance of toxic protein aggregates while preventing the inappropriate consumption of functional brain tissue. Current Alzheimer's interventions may succeed or fail based on whether they can restore this delicate balance. The mechanistic clarity provides promising targets for next-generation therapeutics, though translating these insights into effective treatments will require precision approaches that distinguish beneficial from harmful microglial activities across disease stages.