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Introduction Microglia, the primary immune cells in the brain, play multifaceted roles in Alzheimer's disease (AD). Microglia can potentially mitigate the pathological progression of AD by clearing amyloid beta (Aβ) deposits in the brain and through neurotrophic support. In contrast, disproportionate activation of microglial pro-inflammatory pathways, as well as excessive elimination of healthy synapses, can exacerbate neurodegeneration in AD. The challenge, therefore, lies in discerning the precise regulation of the contrasting microglial properties to harness their therapeutic potential in AD.
Lepiarz‐Raba et al. (Mon,) studied this question.