| Co-Investigator(Kenkyū-buntansha) |
WATANABE Kazuo School of Medicine, Assistant, 医学部, 助手 (60107828)
UEKI Takatoshi School of Medicine, Assistant, 医学部, 助手 (60317328)
OHNO Koji School of Medicine, Associate Professor, 医学部, 助教授 (90263277)
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| Budget Amount *help |
¥13,700,000 (Direct Cost: ¥13,700,000)
Fiscal Year 2002: ¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2001: ¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2000: ¥7,300,000 (Direct Cost: ¥7,300,000)
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| Research Abstract |
In order to prevent people from neurnal diseases, such as brain vascular diseases and Alzheimer disease, it is needed to analyze the mechanisms of neuronal cell death in detail. However, it is well known that there are different aspects in neuronal cell death depending on the causes and where it happens. In this study, using various animal models, we tried to elucidate the mechanisms of various neuronal cell death. First, using a gerbil 3-min ischemic model, we revealed that protective effect of prosaposin-derived 18-mer peptide on slowly progressive neuronal degeneration after brief ischemia. Furthermore, we succeeded to clone a new gene (Kjr). This gene codes a new protein, which can bind bone morphogenic proteins (BMP). Since the function of BMPs in the central nervous system is still unclear, this discovery may be important in this field. In addition, using in situ hybridization and immunohistochemistry, we investigated the localization of this protein, and found that this protein is expressed in astrocytes throughout the central nervous system. Especially, astrocytes in neurogenetic regions, such as the dentate grurs of the hippocampus and the subventricular zone, intensely expressed this protein. Now we are making knock out mice for this gene. Hereafter, we would like to analyze the role of this gene in ischemic conditions.
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