This is consistent with previous findings that proinflammatory molecules can cause the progression of brain deficits [77], and IL-17 reportedly initiates the onset of synaptic and cognitive impairments in the early stages of Alzheimer’s disease [78], a process that may be mediated by activation of IL-17 receptors and MAPK [79]. Here, IL17A is linked to early-onset autosomal dominant Alzheimer disease.