Purpose The lack of occlusal support is an epidemiological risk factor linked to Alzheimer's disease. This study sought to assess the relationship between amyloid β (Aβ) deposition and the lack of occlusal support in amyloid precursor protein (APP) knock-in mice. Methods Sixteen experimental animals were divided into two groups. The upper molars were extracted in the extraction group (group E), and a sham operation was performed in the control group (group C). The Morris water maze test was performed 4 months after the tooth extraction. Aβ immunohistochemical staining and Nissl staining of the hippocampus were performed. Hippocampal plasma corticosterone and Aβ protein levels were measured. Results In the maze task, the escape latency was significantly longer in group E than in group C. In the probe trials, the time elapsed in the target quadrant was significantly shorter in group E than in group C. The number of hippocampal neurons decreased in group E. There was no significant difference in the plasma corticosterone levels between the two groups, indicating that there was no effect of chronic stress on the behavioral results. Hippocampal Aβ40 and Aβ42 protein levels and Aβ deposition areas by immunohistochemical staining were not significantly different between the two groups. Conclusions Aβ deposition was not increased in the hippocampus of molarless APP knock-in mice. As such, it appears that cognitive impairment due to a lack of occlusal support was not related to Aβ deposition.
