Zhang et al. reported that microglial CD11b is critical for the neurotoxicity induced by β-amyloid (Aβ), the main component of senile plaques in AD, since CD11b knockout significantly attenuates Aβ-induced microglial activation, superoxide production, and neurodegeneration in both in vitro and in vivo conditions [17]. Here, ITGAM is linked to Senile plaques.