Specific microglial subpopulations demonstrate neuroprotective functions by actively suppressing neuroinflammation and preventing tau and amyloid protein aggregation in Alzheimer's disease models. These resident immune cells appear to maintain synaptic integrity and preserve cognitive function through targeted anti-inflammatory responses. This discovery builds on decades of research showing microglia's dual role in neurodegeneration — while some activated microglia contribute to brain damage, others serve protective functions that researchers are only beginning to understand. The therapeutic implications are substantial, as current Alzheimer's treatments focus primarily on clearing protein plaques rather than enhancing the brain's natural defense mechanisms. However, translating these findings from laboratory models to human patients remains challenging, particularly given the complexity of microglial activation states and their varying responses across different disease stages. The research suggests that future treatments might focus on selectively promoting beneficial microglial responses rather than broadly suppressing immune activity. This represents a potential paradigm shift from targeting disease symptoms to amplifying endogenous protective mechanisms, though clinical validation will require extensive human trials to confirm safety and efficacy.