Abstract
A systemic effect of dysfunctional mastication has been suggested as a possible epidemiological risk factor for senile dementia. In recent years, we have evaluated the effects on cognitive function deficits in SAMP8 mice. Aged mice with dysfunctional mastication showed significantly reduced learning ability in a water maze test compared with age-matched control mice, whereas there was no difference between control and molarless young adult mice. Immunohistochemical analysis revealed that in the CA1 region of the hippocampus the molarless condition not only enhanced the age-dependent increase in the density and hypertrophy of GFAP-labeled astrocytes, it decreased the density of Fos-positive neurons and Nissl-stained neurons, or the amount of acetylcholine (ACh) release in the hippocampus, in the same manner. There was a similar age-dependent decrease in choline acetyltransferase in the medial septal nucleus. Furthermore, dysfunctional mastication induced an increase in plasma corticosterone levels. The findings suggest that dysfunctional mastication in aged SAMP8 mice causes abnormalities in the hippocampus through stress, leading to deficits in learning and memory.
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Kazuko, W. et al. (2008). Involvement of Dysfunctional Mastication in Cognitive System Deficits in the Mouse. In: Onozuka, M., Yen, CT. (eds) Novel Trends in Brain Science. Springer, Tokyo. https://doi.org/10.1007/978-4-431-73242-6_7
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DOI: https://doi.org/10.1007/978-4-431-73242-6_7
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