These in vivo observations, supported by the in vitro studies demonstrating that fibrillar β-amyloid can activate the classical [11, 12] and alternative [13] complement pathways and that the complement activation fragment C5a is chemotactic for microglia [14], led to the hypothesis that the complement activation triggered by fibrillar ß-amyloid contributes to the inflammatory reaction that can play a detrimental role in the progression of the later stages of Alzheimer's disease [15]. This evidence concerns the gene C5 and Alzheimer disease.