These findings are supported by studies in humans showing that chronic systemic inflammatory conditions, such as rheumatoid arthritis, increase risk for developing AD through sustained increases in IL-1β, IL-6, TNF-α, and C-reactive protein (CRP) levels, which can cross the blood brain barrier and directly impact brain Aβ metabolism or impact Aβ in the periphery which then interacts with central Aβ pools (Wang et al., 2017). The gene discussed is CRP; the disease is Alzheimer disease.