1988 Fiscal Year Final Research Report Summary
Early changes and pathogenesis of primitive senile plaque
| Project/Area Number |
62570484
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Psychiatric science
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| Research Institution | Niigata University |
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Principal Investigator |
TAKEDA Shigeki Niigata University, Brain Research Institute, Research Associate, 脳研究所, 助手 (90134957)
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| Co-Investigator(Kenkyū-buntansha) |
IKUTA Fusahiro Niigata University, Brain Research Institute, Professor, 脳研究所, 教授 (20018592)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Senile plaque / Primitive senile plaque / Amyloid / Periodic acid-methenamine silver stain / Senile dementia of Alzheimer type / 老年期痴呆 |
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| Research Abstract |
1) We have studied the early change of the primitive senile plaque using the serial ultrathin sections stained by periodic acid-methenamine silver (PAM) method. the epoxy-embedded thin section for light-microscopy revealed more delicate details of the amyloid component in the senile plaque. The next ultrathin section for electron-microscopy showed positive silver gains on the amyloid filaments and amyloid-like substance among the neuronal and glial processes. On the other hand, it was difficult to identify primitive senile plaque-like structure only by conventional electron-microscopy without pam stained electron-microscopy. Primitive senile plaque-like structure was composed of neurites, glial processes and pam positive amyloid-like filaments. The last was almost 10nm in diameter and ran sparsely and irregularly between neurites. We consider that they are important ans suggestive findings for the pathogenesis of the primitive senile plaque.
2) We have studied the significance of senile plaque in the autopsied brain using by pam stain. One of many examined cases have characteristic histopathological pictures; (1) Numerous senile plaques and moderate neuronal cell loss in the cerebral cortex, (2) a few neurofibrillary tangles in the hippocampus, and (3) well preserved neuron in the subcortical gray matter.
Recently, terry et al. proposed a new disease concept, "SDAT without neocortical NFT_s". The histopathology of the cerebral cortex in our patient was very similar to those observed in their patients. However, the above authors did not mention any subcortical changes. Tentatively, we classified the present case as denile dementia with numerous neocortical senile plaques and preserved subcortical nuclei. Although we feel that further clinicopathological studies are necessary, the present case appears to be somewhat different from the well known picture of sdat from a neuropathological viewpoint.
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