IL1B and Alzheimer disease: In contrast, children and young adults exhibited a wide spectrum of neurodegenerative disorders, such as increases in microglial activation (CD68 and CD163), elevated pro-inflammatory proteins (COX-2 and IL-1β) and the innate immunity receptor CD14, accumulated AD or PD proteins (Aβ42 and α-synuclein), oxidative stress in frontal and infratentorial neurons and microglia (8-hydroxydeoxyguanosine (8-OHdG) and nitrotyrosine), and frontal BBB impairment, as well as the reduction of the neuroprotective cellular prion protein (PrPC) in the frontal cortex [42].