In the last decade, periodontitis has been reported as a risk factor for the development of Alzheimer's disease (AD). Recently, it has been suggested that gingipain, a toxic protease secreted by Porphyromonas gingivalis, plays critical roles in host colonization, inactivation of host defenses, nutrient acquisition and tissue destruction. However, we do not have any evidence that gingipain exacerbates features of AD and affects the level of TREM2 via amyloid β -protein (Aβ). In this work, it is examined that gingipain helps the brain colonization of P. gingivalis and increases the production of Aβ(1-42). The work measures the concentrations of bacterial endotoxin and the concentrations of Aβ(40 and 42) in the brains of different groups of P. gingivalis-inoculated Tg mice. CoIP (Co-Immunoprecipitation) is used to prove the interactions between amyloid-β and TREM2. Also, the work employs the knock-out of TREM1 and TREM2 in mice' s brains. All mice with different knock-out conditions are divided into four groups, 'with TREM1 & with TREM2', 'with TREM1 & without TREM2', 'without TREM1 & with TREM2', and 'without TREM1 & without TREM2', and gingipain is induced into the brains of all mice. Furthermore, the mice are divided into 4 groups with one TREM-1 knock-out, one TREM2 knock-out, one both TREM1 and TREM2 knock-out, and one no knock-out to do 3 mouse behavior experiments (maze, boxes with road A with electron shock and road B, and 2 boxes covered with different odor, one with food).