| Project/Area Number |
06670975
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Juntendo University |
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Principal Investigator |
ARAI Heii Juntendo University, School of Medicine, Lecturer, 医学部, 講師 (50167988)
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| Co-Investigator(Kenkyū-buntansha) |
KIMURA Michihiro Juntendo University, School of Medicine, Doctor, 医学部, 助手 (50234381)
TAKAHASHI Tadashi Juntendo University, School of Medicine, Doctor, 医学部, 助手 (30236294)
IWAMOTO Norihiko Juntendo University, School of Medicine, Lecturer, 医学部, 講師 (60211067)
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| Project Period (FY) |
1994 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | memory / nitric oxide / Alzheimer-type dementia |
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| Research Abstract |
The aim of the present project is to understand the role of nitric oxide in the mechanism of long term potentiation or memory process by using postmortem human brains obtained from patients with Alzheimer-type dementia (ATD).
The main findings are as follows ;
1. Immunohistochemical double staining studies revealed that nitric oxide synthase (NOS)-like immunoreactivity (LI) was not co-localized in the choline acetyltransferase-positive neurons in the bucleus basalis of Meynert. More-over, NOS-LI was not detected so far in the senile plaques in the ATD brains.
2. NOS-positive neurons were found in hippocampus in postmortem brains. The concentration of glutamate was significantly redused in hippocampus and cortical areas. These glutamate abnormality might affect the NOS activity in the neurons which may disturb the long term potentiation in hippocampal neurons in ATD brains.
3. The investigations of DNAs obtained from 50 ATD patients an 48 control subjects by using the method of poly-merase chain reaction (PCR)-single stranded conformation polymorphism (SSCP) disclosed that there was no point mutation or polymorphism in the exon 2,13 or 14 of NOS gene. These findings suggest the NOS gene is not the focus for the etiology of Alzheimer's discase.
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