Tooth loss might not alter molecular pathogenesis in an aged transgenic Alzheimer's disease model mouse

Background and objective Previous studies have reported that tooth loss is a risk factor of Alzheimer's disease (AD). However, the association between tooth loss and cognition and the impact of tooth loss on the molecular pathogenesis of AD remain elusive. In this study, we tested the effect of...

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Veröffentlicht in:Gerodontology 2016-09, Vol.33 (3), p.308-314
Hauptverfasser: Oue, Hiroshi, Miyamoto, Yasunari, Koretake, Katsunori, Okada, Shinsuke, Doi, Kazuya, Jung, Cha-Gyun, Michikawa, Makoto, Akagawa, Yasumasa
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Sprache:eng
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Zusammenfassung:Background and objective Previous studies have reported that tooth loss is a risk factor of Alzheimer's disease (AD). However, the association between tooth loss and cognition and the impact of tooth loss on the molecular pathogenesis of AD remain elusive. In this study, we tested the effect of tooth loss on learning and memory and on the molecular pathogenesis of AD in an aged AD model mice. Materials and methods We divided 14‐month‐old amyloid precursor protein (APP) transgenic mice, an AD model mouse line, into upper molar extracted group (experimental) and molar intact group (control). At 18 months old, we analysed not only the changes of amyloid‐beta (Aβ), pyramidal cells in the brain but also the learning and memory ability with step‐through passive avoidance test. Results The amount of Aβ and the number of pyramidal cells in the hippocampus were not significantly different between the experimental and control group. Similarly, the difference of learning and memory ability could not be distinguished between the groups. Conclusion Neither molecular pathogenesis of AD nor associated learning and memory were aggravated by tooth loss in these mice. The limited results of this study which used the aged mice may help the dental profession to plan and explain treatments to patients with AD, which must be designed while taking into account the severity of the AD symptoms.
ISSN:0734-0664
1741-2358
DOI:10.1111/ger.12153