Microglia also respond to increased Aβ levels by proliferating and upregulating CD68 and Trem2. Partial depletion of microglia indicated that the surviving phagocytic microglia, rather than their absence, likely drive the age-dependent effect on glutamate release that becomes exacerbated in Alzheimer’s disease. This evidence concerns the gene CD68 and early-onset autosomal dominant Alzheimer disease.