Acute reduction triggers increased microglial phagocytosis, slowing amyloid deposition in mice.

Heterozygous genetic variants within the gene show a strong association with increased Alzheimer's disease (AD) risk. Amyloid beta-depositing mouse models haploinsufficient or null for have identified important relationships among TREM2, microglia, and AD pathology; however, results are challenging to interpret in the context of varying microglial phenotypes and disease progression. We hypothesized that acute reduction may alter amyloid pathology and microglial responses independent of genetic deletion in mouse models.