2007 Fiscal Year Final Research Report Summary
STUDY OF THE MECHANISM OF NEURONAL CELL DAMAGE IN DEMENTIA FOR EARLY DIAGOSIS
| Project/Area Number |
18591303
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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 | Sapporo Medical University |
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Principal Investigator |
SOHMA Hitoshi Sapporo Medical University, SCHOOL OF MEDICINE, ASSOCIATE PROFESSOR (70226702)
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| Co-Investigator(Kenkyū-buntansha) |
KOKAI Yasuo SAPPORO MEDICAL UNIVERSITY, SCHOOL OF MEDICINE, PROFESSOR (20178239)
IKEDA NOZOMU SAPPORO MEDICAL UNIVERSITY, SCHOOL OF HEALTH SCIENCES, PROFESSOR (00274944)
MURAKAMI Shinji HOKKAIDO UNIVERSITYGRADUATE, SCHOOL OF HEALTH SCIENCES, PROFESSOR (30142756)
SAITO Toshukazu SAPPORO MEDICAL UNIVERSITY, SCHOOL OF MEDICINE, PROFESSOR (50128518)
YASUYOSHI Naishiro SAPPORO MEDICAL UNIVERSITY, SCHOOL OF MEDICINE, ASSISTANT PROFESSOR (80347161)
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| Project Period (FY) |
2006 – 2007
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| Keywords | dementia / Alzheimer's disease / Ca^<2+>-stress / annexin A5 / proteomics / plasma / biomarker / neuronal cell |
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| Research Abstract |
In dementia such as Alzheimer's disease (AD) morphological change due to neuronal cell apoptosis is observed in the brain. The cell damage in dementia has been reported to be caused by functional disorder of mitochondria and microsomes. Intracellular elevation of Ca^<2+> is involved in the pathophysiology of AD due to accumulation of peptide A. AD is often diagnosed at a moderately advanced stage. Early detection is required for early treatment. In this study we aimed to investigate molecular markers representing AD. We first analyzed secreted proteins from culture cells (human neuroblastoma NB-1 and rat glioma C6 cells), induced by Ca^<2+>-damage with A23187. Then, we analyzed the protein in blood plasma of dementia patients. As the blood-brain barrier strictly limits transport into the brain through both physical (tight junctions) and metabolic (enzymes) barriers and relatively hydrophobic materials tends to go through the barrier, we isolated the lipid liposome (PC : PS=9 : 1) binding proteins. Annexiss A5, A2 and fetuin were identified after separation on 2D-gel with LC-MS. As annexin A2 is highly expressed in blood cells, we focused on annexin A5. In the next step, blood plasma level of annexin A5 was measured using sandwich ELISA with AD, other dementia patients and controls. The level of plasma annexin A5 was 3.92±2.08 ng/ml in AD, while that in control was 0.87±0.21 ng/ml. The plasma annexin A5 level tended to increase with decreasing level of Hasegawa dementia scale (HDS-R) score. On the other hand, plasma annexin A5 level tended to be high (0.87±1.29 ng/ml) in vascular dementia patients, although not significantly higher than in controls. The physiological role of annexin A5 in the etiology of AD is next to be clarified.
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[Presentation] (Symposium)2007
Author(s)
Kokai, Y
Organizer
Neuro2007
Place of Presentation
Yokohama, Japan
Year and Date
20070910-12
Description
「研究成果報告書概要(欧文)」より
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