Subsequent work treating mouse models of AD with a C5a receptor antagonist resulted in a 50–70% decrease in pathological markers suggesting that the detrimental effects of complement activation in the brain were predominantly mediated by the proinflammatory C5a fragment generated upon the activation of the complement cascade through the cleavage of C5 (to C5a and C5b) [23]. The gene discussed is C5; the disease is Alzheimer disease.