| Project/Area Number |
05454314
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Psychiatric science
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| Research Institution | Hyogo College of Medicine |
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Principal Investigator |
KOHO Miyoshi Hyogo College of Medicine The faccult of Medicine Professor, 医学部, 教授 (10068447)
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| Co-Investigator(Kenkyū-buntansha) |
古橋 淳夫 兵庫医科大学, 医学部, 助手 (30238688)
湖海 正尋 兵庫医科大学, 医学部, 助手 (70258143)
植木 昭紀 兵庫医科大学, 医学部, 講師 (30203425)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1993: ¥4,500,000 (Direct Cost: ¥4,500,000)
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| Keywords | Animal Model of Alzheimer's Disease. / Basal Forebrain / Tacrine / Amiridine / SDZ-ENA713 / Entorhinal Cortex / AETT / Leupeptin / SDZ-ENA713 / リポフスチン / プロテアーゼ阻害物質 / 痴呆モデル動物 |
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| Research Abstract |
It is necessary to have a good animal model for the research of the pathogenesis of Alzheimer's disease, as well as for the exploration of nootropic drugs.
1) Characteristics of learning impairment and ameriolating effects of cholinergic drugs were studied in the basal forebrain lesioned rats. Impairment of acquisition and retention were demonstrated in the passive avoidance procedure. Cholinesterase inhibitors, tetrahydroaminoacridine (tecrine), amiridine, and SDZ-ENA713 caused significant ameriolation of learning impairment caused by bilateral basal forebrain lesion.
2) Bilateral entorhinal cortex lesions, caused by the stereotaxic iboteinic acid injection, caused significant impairment of learning ability, especially acquisiton in passive and active avoidance procedures.
3) Accumulation of neuronal lipofuscin, induced experimentally by tocopherol deficiency, tellurium intoxication, AETT intoxication, caused significant learning disability in rats.
4) Persistent intraventricular injection of leupeptin, protease inhibitor, caused degeneration and swelling of neurites and axons in rat brains. The changes of neuronal processes were closely similar to the neuritic changes in the senile plaques of Alzheimer's disease.
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