The local concentration of Aβ peptides produced by these injections is likely much higher than occurs in AD, and the sudden increase in Aβ is non-physiologic; however, the near-complete absence of Aβ-induced microglial activation in PARP-1-/- mice or in wt mice treated with a PARP-1 inhibitor supports the idea that PARP-1 activity is essential for microglial activation in response to Aβ. The gene discussed is PARP1; the disease is Alzheimer disease.