2000 Fiscal Year Final Research Report Summary
Deposition mechanism and gene expression of amyloid P component in brains of Alzheimer-type dementia
| Project/Area Number |
09671007
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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 |
ICHIMIYA Yousuke Juntendo Univ.Associate Professor, 医学部, 助教授 (10184631)
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| Co-Investigator(Kenkyū-buntansha) |
KIMURA Michihiro Juntendo Univ.Assistant Professor, 医学部, 講師 (50234381)
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| Project Period (FY) |
1997 – 2000
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| Keywords | Alzheimer type dementia / amyloid P component amyloiddeposition / in situ hybridization / cerebrospinal fluid / mRNA distribution / serum amyloid A / 血清アミロイドA |
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| Research Abstract |
1. We performed in situ hybridization histochemistry and immunohisotochemistry in AD and human control brains. Our in situ hybridization study showed that APC mRNA was expressed in the neural cells in all cortical layers. Immunohistochemistry also showed that APC- immunorectivity was widely positive in the neural cells in all cortical layers in both subjects. These results suggest that APC which has deposited in the AD brain is synthesized in brain itself, not in liver. However, there is no difference between the distribution of APC gene expression in AD and that in control brains.
2. We evaluated the APC levels in CSF of patients with ATD and normal control subjects. There was no significant difference in the APC levels between the AD group and normal control group. However, among AD patients, cognitive function was rated using MMSE and was correlated with APC levels. These results suggest that measurement of APC levels in CSF can be useful for assessing the degree of cognitive impairmentin ATD patients.
3. We measured the Tau, soluble amyloid precursor protein(sAPP) levels in CSF, which were candidate diagnostic marker of ATD.Both of them were no correlation with APC levels. This result suggest the deposition mechanism of APC may be different from the depositon mechanism of Tau and sAPP.
4. We also measured serum amyloid A component(SAA), which is the marker of inflammation and exist in the amyloid depositon in the patient of systemic amyloidosis. It was not correlated with APC.This result suggest that the deposition mechanism of APC not relate with inflammation directly and differ from the mechanism of systemic amyloidosis.
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