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Updated: May 31, 2026

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
Published on: July 29, 2018
Occlusal disharmony increases amyloid-β in the rat hippocampus
1Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama, 700-8558, Japan. dekuni7@md.okayama-u.ac.jp
Abstract:
Amyloid-β plays a causative role in Alzheimer's disease. Occlusal disharmony causes chronic psychological stress, and psychological stress increases amyloid-β accumulation. The purpose of the present study was to investigate whether occlusal disharmony-induced psychological stress affects the accumulation of amyloid-β and its related gene expressions in the rat hippocampus. Eight-week-old male Wistar rats (n = 18) were divided into three groups of six rats each: (1) a control group that received no treatment for 8 weeks; (2) an occlusal disharmony group that underwent cutoff maxillary molar cusps for 8 weeks; and (3) a recovered group that underwent cutoff maxillary molar cusps for 4 weeks followed by recovery for 4 weeks. Occlusal disharmony increased plasma corticosterone levels in a time-dependent manner. Levels of amyloid-β 40 and 42, glucocorticoid receptor (Gr) protein, and cleaved caspase 3 (Casp3) as well as gene expressions of amyloid precursor protein, beta-secretase, Casp3, and Gr in the hippocampus in the occlusal disharmony group were significantly higher than those in the control group (P < 0.016). These findings were significantly improved by recovery of occlusion (P < 0.016). These results indicate that psychological stress induced by occlusal disharmony reversibly induces amyloid-β 40 and 42 in the rat hippocampus through the glucocorticoid signal.

