Since primary neurons derived from C5aR1KO mice showed no C5a-induced loss of MAP-2, taken together these data provide evidence that neuronal C5aR1 is the receptor mediating the C5a induced neuronal damage and suggests that another beneficial consequence of C5aR1 antagonists in the context of AD is suppressing detrimental neuronal C5a-C5aR1 signaling. The gene discussed is MAP2; the disease is Alzheimer disease.