| Project/Area Number |
13470451
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
矯正・小児・社会系歯学
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
TANNE Kazuo Graduate School of Biomedical Sciences : professor, 大学院・医歯薬学総合研究科, 教授 (30159032)
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| Co-Investigator(Kenkyū-buntansha) |
KAKU Masato University Dental Hospital : research associate, 歯学部附属病院, 助手 (10325194)
KAWATA Toshitsugu University Dental Hospital : assistant professor, 歯学部附属病院, 講師 (80281161)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥10,900,000 (Direct Cost: ¥10,900,000)
Fiscal Year 2002: ¥4,600,000 (Direct Cost: ¥4,600,000)
Fiscal Year 2001: ¥6,300,000 (Direct Cost: ¥6,300,000)
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| Keywords | Mastication / op / op mouse / M-CSF / hippocampus / Amyloid β / Alzheimer's disease / pyramidal cell / βアミロイドタンパク / 神経細胞 / 歯の喪失 / 軟性食品 / 神経脱落 |
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| Research Abstract |
Amyloid β(Aβ) protein of senile plaques (SPs) is a neuropathological change which characterize Alzheimer's disease (AD), and its deposition and neuron loss are essential for the pathological cascade of the disease. Although the mechanism of Aβ deposition still remains unclear, it is suggested that a clearance activity for the Aβ protein may be impaired in AD's brain. Previous studies demonstrated that microglia could remove Aβ by releasing a metalloprotease or by phagocytosis, suggesting that microglia may play an important role in preventing Aβ deposition in the central nervous system (CNS). On the other hand, it was reported that the number of microglia was reduced in osteopetrotic (op/op) toothless mice resulting from the lack of functional macrophage colony-stimulating factor (M-CSF). It was also exhibited that impairment of masticatory function caused degeneration of hippocampal neurons. The present study was thus designed to examine the Aβ deposition and the number of hippocampal neurons in the brain of op/op mice. A number of mature Sps were detected in the cerebral cortex, hippocampus, amygdala and hypothalamus in op/op mice, however, no quantitative evidence of Aβ deposition was observed in normal mice. Moreover, the number of pyramidal cells in the CA1, and CA3 regions was significantly reduced in op/op mice than in the controls. It is shown that Aβ deposition and reduced mastication influence the neuron loss and expression of SPs may be in part regulated by microglia under a physiological conditions.
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