IL17A and Alzheimer disease: It was found that in the course of AD neutrophils accumulate near Aβ and disrupt blood flow in the brain, helper TCD4+ (Th17) lymphocytes synthesize interleukin-17 (IL-17), which contributes to cognitive impairment, T cytotoxic CD8+ lymphocytes disrupt synaptic plasticity, B lymphocytes increase the accumulation of senile plaques or microglial dysfunction, and NK cells, through interaction with microglia, contribute to the synthesis of inflammatory mediators [28].