| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Haruyasu Guma University, School of Medicine, Professor, 医学部, 教授 (00158114)
MIYAKAWA Taihei Kumamoto University, School of Medicine, Professor, 医学部, 教授 (90040542)
ARAKI Norie Kumamoto University, School of Medicine, Assistant, 医学部, 助手 (80253722)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
Accumulation of amyloid β protein (Aβ) in the brain is the primary event in the pathological process in Alzheimer's disease (AD). Investigation of Aβ metabolism is indispensable for inquire into cause of AD. Several researchers have detected enzymes associated with the metabolism. On the other hand, the metabolism in human tissues except brains have been scarcely examined.
In this study, immunoreactions to anti-AβC-terminal, anti-AβN-terminal, and anti-Aβ17-24 (4G8) were found in non-neural human tissues except brains such as heart, lung, liver, kidney, spleen, pancreas, ileum, and skin. It was suggested that the immunoreactions result from cross reaction, because they were not detected by biochemical methods.
Some immunological studies using anti-AβC terminal have found the presence of Ap in neurons. It is supported by our finding that immunoreaction in neurons to 4G8 was detected using immunohistochemical methods. However, we did not identify the N-terminal of Aβ existing in neurons, suggesting the possibility that such Aβ is not modified at N-terminal or that anti-AβN-terminal, which we used in this study, can not recognize the N-terminal of Aβ within neurons.
We did not find transfer of serum injected-Aβ into the parenchyma of rat brains at least during 30 days, using immunohistochemical examination. Since, it is possible that the transfer occur in aged rats, different animals, or longer exposure of Aβ, further studies will be necessary.
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