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Senile dementia and amyloid protein. Jun TATEISHI 1 , Tetsuyuki KITAMOTO 1 , Koji OGOMORI 1 1Department of Neuropathology, Neurological Institute Faculty of Medicine, Kyushu University pp.1021-1026
Published Date 1988/12/10
DOI https://doi.org/10.11477/mf.1431906249
  • Abstract
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Senile dementia, especially Alzheimer's disease, is a cerebral amyloidosis, which is mainly consisted of β-protein. Two amyloid structures, amyloid angiopathy and senile plaques, are closely related in some brains, but not in others. EM study of amyloid angiopathy revealed that amyloid fibrils were produced by pericytes of capillaries and by smooth muscle cells of arterioles. In senile plaques, amyloid fibrils aggregated to form central cores and radiated around the cores. Immunostain using anti-β-protein anti-serum revealed various types of amyloid deposition around blood vessels with or without amyloid angio-pathy, in subependymal and subarachnoidal areas, and in columnar shape in the cerebellar cortex.

Morphologically, senile plaques resemble kuru plaques seen in Creutzfeldt-Jakob disease (CJD) and allied diseases, though the latter plaque consists of prion protein. Immunostain using antisera against both proteins can clearly identify each plaque and increase the incidence of the plaques. All of CJD patients with clinical duration of over one year shows kuru plaques and aged patients with CJD show both plaques independently.


Copyright © 1988, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1243 印刷版ISSN 0001-8724 医学書院

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