Literature DB >> 9838181

Striation is the characteristic neuritic abnormality in Alzheimer disease.

M E Velasco1, M A Smith, S L Siedlak, A Nunomura, G Perry.   

Abstract

In this study, we found that neuropil threads of Alzheimer disease, rather than being continuous filaments along cell processes, show multiple interruptions. They are segmental in nature and therefore appear as striations rather than continuous filaments along the length of the neurite. Neuritic striation is not an artifact of section thickness since the majority of abnormal filament accumulations are extremely short. The dominance of short striations demonstrates that argyrophilic grains, rather than being distinct structures, simply represent a short variant of striation and that longer striations are arbitrarily considered neuropil threads. Ultrastructural examination showed that the intervals between striations lack a cytoskeleton. We suggest that neuritic striations may interrupt the microtubule system functionally blocking fast neuritic transport as well as playing a role in loss of neuronal connectivity. Copyright 1998 Elsevier Science B.V.

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Year:  1998        PMID: 9838181     DOI: 10.1016/s0006-8993(98)01034-8

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  14 in total

Review 1.  Actin dynamics and cofilin-actin rods in alzheimer disease.

Authors:  James R Bamburg; Barbara W Bernstein
Journal:  Cytoskeleton (Hoboken)       Date:  2016-03-01

Review 2.  ADF/Cofilin-actin rods in neurodegenerative diseases.

Authors:  J R Bamburg; B W Bernstein; R C Davis; K C Flynn; C Goldsbury; J R Jensen; M T Maloney; I T Marsden; L S Minamide; C W Pak; A E Shaw; I Whiteman; O Wiggan
Journal:  Curr Alzheimer Res       Date:  2010-05       Impact factor: 3.498

3.  Activated actin-depolymerizing factor/cofilin sequesters phosphorylated microtubule-associated protein during the assembly of alzheimer-like neuritic cytoskeletal striations.

Authors:  Ineka T Whiteman; Othon L Gervasio; Karen M Cullen; Gilles J Guillemin; Erica V Jeong; Paul K Witting; Shane T Antao; Laurie S Minamide; James R Bamburg; Claire Goldsbury
Journal:  J Neurosci       Date:  2009-10-14       Impact factor: 6.167

Review 4.  Cytoskeletal pathologies of Alzheimer disease.

Authors:  James R Bamburg; George S Bloom
Journal:  Cell Motil Cytoskeleton       Date:  2009-08

5.  Is abnormal axonal transport a cause, a contributing factor or a consequence of the neuronal pathology in Alzheimer's disease?

Authors:  Virgil Muresan; Zoia Muresan
Journal:  Future Neurol       Date:  2009-11-01

6.  Mapping cofilin-actin rods in stressed hippocampal slices and the role of cdc42 in amyloid-beta-induced rods.

Authors:  Richard C Davis; Michael T Maloney; Laurie S Minamide; Kevin C Flynn; Matthew A Stonebraker; James R Bamburg
Journal:  J Alzheimers Dis       Date:  2009       Impact factor: 4.472

7.  Incorporation of cofilin into rods depends on disulfide intermolecular bonds: implications for actin regulation and neurodegenerative disease.

Authors:  Barbara W Bernstein; Alisa E Shaw; Laurie S Minamide; Chi W Pak; James R Bamburg
Journal:  J Neurosci       Date:  2012-05-09       Impact factor: 6.167

8.  Amyloid beta dimers/trimers potently induce cofilin-actin rods that are inhibited by maintaining cofilin-phosphorylation.

Authors:  Richard C Davis; Ian T Marsden; Michael T Maloney; Laurie S Minamide; Marcia Podlisny; Dennis J Selkoe; James R Bamburg
Journal:  Mol Neurodegener       Date:  2011-01-24       Impact factor: 14.195

9.  Rapid changes in phospho-MAP/tau epitopes during neuronal stress: cofilin-actin rods primarily recruit microtubule binding domain epitopes.

Authors:  Ineka T Whiteman; Laurie S Minamide; De Lian Goh; James R Bamburg; Claire Goldsbury
Journal:  PLoS One       Date:  2011-06-28       Impact factor: 3.240

10.  β-Secretases, Alzheimer's Disease, and Down Syndrome.

Authors:  Robin L Webb; M Paul Murphy
Journal:  Curr Gerontol Geriatr Res       Date:  2012-02-28
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