C3 and early-onset autosomal dominant Alzheimer disease: Synaptic loss in a mouse model of Alzheimer’s disease has been linked to aberrant expression of C1q which was further shown essential for soluble β amyloid synaptic toxicity [47]; in mice, West Nile virus infection of neurons drives their expression of complement components leading to pruning of pre-synaptic termini, a disease state absent in C1q or C3 knockout mice [50], and remarkably, C3 knockout mice failed to display even synaptic loss leading to neuronal loss and defects in memory observed during normal aging [71].