Accumulation of amyloid-β (Aβ) around cerebral blood vessels is found in more than 80% of Alzheimer's disease (AD) patients, and peripheral Aβ can accumulate in brain triggering degeneration. Recently, periodontitis has been reported positively link to AD, however, the mechanism of peripheral Aβ transport into brain is unclear. we hypothesized that periodontitis may involve in peripheral Aβ transport into brain. In the present study, we aim to examine the expression of Receptor for advanced glycation end products (RAGE) on brain endothelial cells after infection with Porphyromonas gingivalis (P.g.), the major pathogenic bacteria of periodontitis, because RAGE is mediated in transporting peripheral Aβ into brain. The mRNA level and immunofluorescent signal of of RAGE were significantly increased in hCMEC/D3 cells after P.g exposure. The expression of RAGE on CD31-positve endothelial cells were significantly increased in the P.g infected mice compared to control mice. Moreover, Aβ were detected on CD31-positve endothelial cells surrounding cerebral blood vessels in the P.g infected mice. These observations suggested that increased RAGE expression in endothelial cells is involved in Aβ influx into brain after P.g infection.