Literature DB >> 7678852

Hirano bodies accumulate C-terminal sequences of beta-amyloid precursor protein (beta-APP) epitopes.

D G Munoz1, D Wang, B D Greenberg.   

Abstract

Hirano bodies (HB) are cytoplasmic inclusions predominantly found in the CA1 sector of the hippocampus. In Alzheimer's disease they are dislocated to the stratum pyramidale from their normal position in the stratum lacunosum. Hirano bodies are known to contain epitopes related to microfilaments (actin), neurofilaments, and microtubules (tau). In cryostat sections of the hippocampus from both Alzheimer's disease and normal patients, HB were decorated by two antisera raised against different sequences of the cytoplasmic domain of beta-amyloid precursor protein (beta-APP), and two antisera against the beta/A4 sequence of beta-APP, but not by two antisera directed against ectodomain (N-terminal) sequences of beta-APP. Thus, in contrast to dystrophic neurites in plaques, which are decorated by antibodies to either terminus of beta-APP, HB appear to be a site of preferential accumulation of C-terminal fragments of beta-APP, extending to include at least part of beta/A4.

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Year:  1993        PMID: 7678852     DOI: 10.1097/00005072-199301000-00003

Source DB:  PubMed          Journal:  J Neuropathol Exp Neurol        ISSN: 0022-3069            Impact factor:   3.685


  8 in total

Review 1.  Neuropathological alterations in Alzheimer disease.

Authors:  Alberto Serrano-Pozo; Matthew P Frosch; Eliezer Masliah; Bradley T Hyman
Journal:  Cold Spring Harb Perspect Med       Date:  2011-09       Impact factor: 6.915

2.  Modulation of gene expression and cytoskeletal dynamics by the amyloid precursor protein intracellular domain (AICD).

Authors:  Thorsten Müller; Caoimhin G Concannon; Manus W Ward; Ciara M Walsh; Anca L Tirniceriu; Florian Tribl; Donat Kögel; Jochen H M Prehn; Rupert Egensperger
Journal:  Mol Biol Cell       Date:  2006-11-08       Impact factor: 4.138

3.  Association of AICD and Fe65 with Hirano bodies reduces transcriptional activation and initiation of apoptosis.

Authors:  Sangdeuk Ha; Ruth Furukawa; Marcus Fechheimer
Journal:  Neurobiol Aging       Date:  2010-02-04       Impact factor: 4.673

4.  Autophagy contributes to degradation of Hirano bodies.

Authors:  Dong-Hwan Kim; Richard C Davis; Ruth Furukawa; Marcus Fechheimer
Journal:  Autophagy       Date:  2009-01       Impact factor: 16.016

5.  Model Hirano bodies protect against tau-independent and tau-dependent cell death initiated by the amyloid precursor protein intracellular domain.

Authors:  Matthew Furgerson; Marcus Fechheimer; Ruth Furukawa
Journal:  PLoS One       Date:  2012-09-18       Impact factor: 3.240

6.  Transgenic mouse model for the formation of Hirano bodies.

Authors:  Sangdeuk Ha; Ruth Furukawa; Michael Stramiello; John J Wagner; Marcus Fechheimer
Journal:  BMC Neurosci       Date:  2011-10-06       Impact factor: 3.288

7.  Hirano bodies differentially modulate cell death induced by tau and the amyloid precursor protein intracellular domain.

Authors:  William Spears; Matthew Furgerson; John Michael Sweetnam; Parker Evans; Marla Gearing; Marcus Fechheimer; Ruth Furukawa
Journal:  BMC Neurosci       Date:  2014-06-14       Impact factor: 3.288

8.  Hirano body expression impairs spatial working memory in a novel mouse model.

Authors:  Matthew Furgerson; Jason K Clark; Jonathon D Crystal; John J Wagner; Marcus Fechheimer; Ruth Furukawa
Journal:  Acta Neuropathol Commun       Date:  2014-09-02       Impact factor: 7.801

  8 in total

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