These data were confirmed by ELISA experiments, showing significantly less Aβ1-40 and Aβ1-42 deposition, and tau hyperphosphorylation (pT231, AT180) in the soluble and insoluble fractions of brain homogenates from 3xTg-AD mice depleted of CD8 + T cells compared to isotype controls (Fig. 5j, k), while no significant differences were observed in the levels of total tau (Fig. 5l). This evidence concerns the gene CD8A and Alzheimer disease.