In AD mouse models, accumulation of oligomeric Aβ and hyperphosphorylated tau leads to the glial overexpression of several complement components, and molecular inhibition or genetic deletion of complement factors/receptors, such as C3/C3R, C5/C5R, and C1q decrease glial activation, Aβ and hyperphosphorylated tau deposition, and synaptic pruning [7,14,15,16,17]. This evidence concerns the gene MAPT and Alzheimer disease.