In another transgenic AD model, that contains a third “Arctic” mutation in the human APP transgene that accelerates the formation of fibrillar Aß plaques [167], genetic ablation of C5aR1 prevented the loss of neuronal complexity (CA1 region of the hippocampus) and the decline of cognitive performance seen in the C5aR1 sufficient Arctic mice at 10 months of age without any change of plaque accumulation [86]. This evidence concerns the gene C5AR1 and Alzheimer disease.