Ms4a4a loss reprograms amyloid-associated microglia and limits dense-core plaque-associated tau spreading
These findings identify Ms4a4a as a regulator of plaque-associated microglial programs linked to NP-tau accumulation in the amyloid-bearing brain, which supports a model in which AD resilience-associated microglial pathways selectively shape plaque-associated microenvironments that promote downstream tau pathology.