Literature DB >> 8971793

The amino-terminally truncated forms of amyloid beta-protein in brain macrophages in the ischemic lesions of Alzheimer's disease patients.

H Akiyama1, H Kondo, H Mori, F Kametani, T Nishimura, K Ikeda, M Kato, P L McGeer.   

Abstract

We have investigated the cerebral cortex of Alzheimer's disease in which small infarcts are found on postmortem neuropathological examination. In areas that have been subjected to recent ischemia, immunohistochemical staining for amyloid beta-protein (A beta) is much less intense than in the non-ischemic surround. However, the infiltrating brain macrophages contain granules immunopositive for C-terminal fragments of A beta. The immunohistochemical profile indicates that A beta in these granules lacks epitopes in the N-terminal fragments. These data suggest that appropriately stimulated macrophages can phagocytose A beta deposits and that digestion of the N-terminal region is an early consequence of this phagocytosis.

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Year:  1996        PMID: 8971793     DOI: 10.1016/s0304-3940(96)13197-9

Source DB:  PubMed          Journal:  Neurosci Lett        ISSN: 0304-3940            Impact factor:   3.046


  12 in total

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2.  Astrocytes containing amyloid beta-protein (Abeta)-positive granules are associated with Abeta40-positive diffuse plaques in the aged human brain.

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5.  Is TNF a link between aging-related reproductive endocrine dyscrasia and Alzheimer's disease?

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Review 8.  Migration of blood cells to β-amyloid plaques in Alzheimer's disease.

Authors:  Lindsay A Hohsfield; Christian Humpel
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9.  Inflammatory process in Alzheimer's Disease.

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10.  Administration of Amyloid Precursor Protein Gene Deleted Mouse ESC-Derived Thymic Epithelial Progenitors Attenuates Alzheimer's Pathology.

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Journal:  Front Immunol       Date:  2020-08-11       Impact factor: 7.561

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