2023 Fiscal Year Final Research Report
New molecular mechanism of maintain cognitive ability induced by sensory input in oral mucosa wearing with denture
Project/Area Number |
22K21005
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Research Category |
Grant-in-Aid for Research Activity Start-up
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Allocation Type | Multi-year Fund |
Review Section |
0907:Oral science and related fields
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Research Institution | Fukuoka Dental College |
Principal Investigator |
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Project Period (FY) |
2022-08-31 – 2024-03-31
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Keywords | アルツハイマー型認知症 / 口腔粘膜 / 義歯装着 / 咬合感覚入力 |
Outline of Final Research Achievements |
Alzheimer model mice (APPKI(3)) using eight-arm radial test (ERMT), but not at 6months in APPKI(3) mice. The tooth loss upregulated the positive cells of AD-related molecules (amyloid-beta, p-tau in trigeminal mesencephalic nucleus (Vmes)) in APPKI(3) mice , but not in locus coeruleus (LC). The extraction also upregulated the remarked expression of AD-related proteins in hippocampus at 2 and 4 months after extraction compared with control in APPKI(3) mice.Furthermore, the tooth loss dominantly upregulated the positive cells of p-Tau in CA3 of hippocampus at 4 month after extraction compared with control (non-extraction) in APPKI (3) mice. In the in vivo experiments, the recovery of occlusal support resulted in a slight recovery trend in cognitive performance at 2 and 4 months of age using behavioural science tests; there was no change after 6 months of age; the same trend was observed in the in vitro experiments.
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Free Research Field |
歯科
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Academic Significance and Societal Importance of the Research Achievements |
近年、咀嚼、嚥下、及び咬合などの口腔機能の口腔医学的な正常の維持により、認知能低下の予防や改善されることが、臨床の現場で明らかになって来ている。その発症機序とリスク排除に関する明確な医学的検証は必須となっている。認知症の中で最も発症率が高いのはアルツハイマー型認知症であり、発症経路としては、アミロイドβが蓄積されること、同時に異常リン酸化されたタウタンパク質により誘発されることが報告されている。しかし、具体的な治療法はなく、認知症の発症前の段階の軽度認知障害(MCI)での危険・増悪因子を医学的根拠に基づいての排除し認知症の予防や進行の遅延の方法を医学的根拠に基づいて確立することが考えられる。
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