Accordingly, knock-out of CCR5 associated with elevation of CCL2 and CCR2 expression in the brain, resulted in higher susceptibility of mice to LPS treatment, manifesting in more pronounced cognitive impairment, activation of astrocytes, expression of inflammatory enzymes and β-secretase, and Aβ deposition as compared to CCR5 wild-type mice (Hwang et al. 2016). This evidence concerns the gene CCR5 and Cognitive impairment.