VTN and Alzheimer disease: The upregulated profiles of complement proteins in AD brain [61–63] and the demonstrated safety of the suppression of C5a generation or C5aR1 signaling in human patients with inflammatory diseases [64, 65], suggests C5aR1 antagonism would be well tolerated and may slow cognitive decline in AD and other neurodegenerative diseases in which complement activation is excessive or not appropriately regulated.