In order to investigate the effects of β-amyloid (Aβ) deposits on migration of peripheral blood T cells across blood-brain barrier, Aβ_1～42 was stereotaxicly injected into rat hippocampus with reverse peptide Aβ_42～1 as control. After 7 days post-injection, the expression of macrophage inflammatory protein-1α (MIP-1α) and its receptor (CCR5) in peripheral blood T cells was detected by real-time quantitative polymerase chain reaction (RT-qPCR). Brain sections were analyzed with immunofluorescence of CD3, VWF and CCR5. The results showed that Aβ_1～42 deposits in rat brains led to significantly higher expression of MIP-1α in circulating T cells than Aβ_42～1 did, while no increase of CCR5 expression was observed in circulating T cells of Aβ_1～42-injected rats compared to Aβ_42～1-injected rats. Furthermore, the expression of CCR5 was up-regulated by Aβ_1～42 on rat brain microvascular endothelial cells (RBMEC). In addition, T cells were increased in abundance in Aβ_1～42-injected brains compared with Aβ_42～1-injected brains, scattered mainly in cortex and hippocampus. Treatment of Aβ_1～42-injected rats with neutralizing antibody specific for MIP-1α dramatically blocked the enhanced T cells entry into rat brain. The results implied that the interaction between MIP-1α over-expressed in T cells and CCR5 on RBMECs may contribute to the Aβ_1～42-induced circulating T cells migrating across blood-brain barrier.