These findings suggest that at least part of the therapeutic benefit of C5aR1 antagonist seen earlier in mouse models of AD (Fonseca et al., 2009) may result from a direct protection of neurons and support further investigation of the use of such antagonists as part of a therapeutic strategy to slow the progression of AD and other neurological disorders in which complement activation may occur generating C5a in a neuronal environment in humans. This evidence concerns the gene C5 and Alzheimer disease.