For example, C3aR deficiency protects mice against the loss of synapses in neuroinvasive viral infection [37] and C3aR antagonist treatment is protective against the reduction in synaptic density and dendritic complexity in neurodegeneration associated with Alzheimer’s disease [35] but has the opposite effects in the absence of any challenge [35], and intranasal treatment with C3a increases synaptogenesis in the peri-infarct region after focal ischemic injury [33]. The gene discussed is C3AR1; the disease is early-onset autosomal dominant Alzheimer disease.