Previous studies in our lab using the Arctic48 mouse model of AD [19] showed that genetic ablation of C5aR1 completely prevented the loss of neurite complexity and cognitive deficits associated with Alzheimer’s disease, whereas overexpression of C5a by a transgene under the GFAP promoter in the same mouse model seems to accelerate hippocampal-dependent spatial memory deficits [20, 21]. This evidence concerns the gene C5 and early-onset autosomal dominant Alzheimer disease.