C3 and Alzheimer disease: Importantly, nuclear factor of kappa-light-chain-enhancer of activated B cells (NF-κB) hyperactivation due to inhibitor of κB kinase (IKK) knockout (KO) results in complement expression by astrocytes because C3 protein secretion is driven by NF-κB activation in these cells, and such responses worsen Aβ-associated pathology, with reduced numbers of synapses and shortened dendritic lengths, and impaired synaptic functions, due to reduced microglial Aβ phagocytosis in AD mouse models (42, 43).