To further explore the role of the TGF‐β signaling pathway in mediating the beneficial effects of microglial Hrh4 deletion in AD mice, we quantified microglial Aβ phagocytic capacity in vivo following injection of Lenti–scr‐shRNA, Lenti–Hrh4–shRNA, and/or Lenti–Tgf‐βr1–shRNA into the cortex and hippocampus (CA1 and CA3 regions) of aged APP/PS1 mice (Figure8A). Here, TGFBR1 is linked to Alzheimer disease.