Activated microglia and astrocytes are also central sources of the complement proteins, particularly C1q and C3 proteins, which in physiological conditions regulate neuronal development by suppressing weak synapses, but if aberrantly expressed, exacerbate synaptic derangements and central inflammation, contributing to the cognitive and mood decline associated with aging or to neurodegenerative disorders, i.e., Alzheimer’s disease (91, 92). Here, VTN is linked to early-onset autosomal dominant Alzheimer disease.