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The Beta-Amyloid Protein of Alzheimer's Disease: Communication Breakdown by Modifying the Neuronal Cytoskeleton

Alzheimer's disease (AD) is one of the most prevalent severe neurological disorders afflicting our aged population. Cognitive decline, a major symptom exhibited by AD patients, is associated with neuritic dystrophy, a degenerative growth state of neurites. The molecular mechanisms governing neu...

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Autores principales: Mokhtar, Sara H., Bakhuraysah, Maha M., Cram, David S., Petratos, Steven
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3876695/
https://www.ncbi.nlm.nih.gov/pubmed/24416616
http://dx.doi.org/10.1155/2013/910502
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author Mokhtar, Sara H.
Bakhuraysah, Maha M.
Cram, David S.
Petratos, Steven
author_facet Mokhtar, Sara H.
Bakhuraysah, Maha M.
Cram, David S.
Petratos, Steven
author_sort Mokhtar, Sara H.
collection PubMed
description Alzheimer's disease (AD) is one of the most prevalent severe neurological disorders afflicting our aged population. Cognitive decline, a major symptom exhibited by AD patients, is associated with neuritic dystrophy, a degenerative growth state of neurites. The molecular mechanisms governing neuritic dystrophy remain unclear. Mounting evidence indicates that the AD-causative agent, β-amyloid protein (Aβ), induces neuritic dystrophy. Indeed, neuritic dystrophy is commonly found decorating Aβ-rich amyloid plaques (APs) in the AD brain. Furthermore, disruption and degeneration of the neuronal microtubule system in neurons forming dystrophic neurites may occur as a consequence of Aβ-mediated downstream signaling. This review defines potential molecular pathways, which may be modulated subsequent to Aβ-dependent interactions with the neuronal membrane as a consequence of increasing amyloid burden in the brain.
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spelling pubmed-38766952014-01-12 The Beta-Amyloid Protein of Alzheimer's Disease: Communication Breakdown by Modifying the Neuronal Cytoskeleton Mokhtar, Sara H. Bakhuraysah, Maha M. Cram, David S. Petratos, Steven Int J Alzheimers Dis Review Article Alzheimer's disease (AD) is one of the most prevalent severe neurological disorders afflicting our aged population. Cognitive decline, a major symptom exhibited by AD patients, is associated with neuritic dystrophy, a degenerative growth state of neurites. The molecular mechanisms governing neuritic dystrophy remain unclear. Mounting evidence indicates that the AD-causative agent, β-amyloid protein (Aβ), induces neuritic dystrophy. Indeed, neuritic dystrophy is commonly found decorating Aβ-rich amyloid plaques (APs) in the AD brain. Furthermore, disruption and degeneration of the neuronal microtubule system in neurons forming dystrophic neurites may occur as a consequence of Aβ-mediated downstream signaling. This review defines potential molecular pathways, which may be modulated subsequent to Aβ-dependent interactions with the neuronal membrane as a consequence of increasing amyloid burden in the brain. Hindawi Publishing Corporation 2013 2013-12-12 /pmc/articles/PMC3876695/ /pubmed/24416616 http://dx.doi.org/10.1155/2013/910502 Text en Copyright © 2013 Sara H. Mokhtar et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Mokhtar, Sara H.
Bakhuraysah, Maha M.
Cram, David S.
Petratos, Steven
The Beta-Amyloid Protein of Alzheimer's Disease: Communication Breakdown by Modifying the Neuronal Cytoskeleton
title The Beta-Amyloid Protein of Alzheimer's Disease: Communication Breakdown by Modifying the Neuronal Cytoskeleton
title_full The Beta-Amyloid Protein of Alzheimer's Disease: Communication Breakdown by Modifying the Neuronal Cytoskeleton
title_fullStr The Beta-Amyloid Protein of Alzheimer's Disease: Communication Breakdown by Modifying the Neuronal Cytoskeleton
title_full_unstemmed The Beta-Amyloid Protein of Alzheimer's Disease: Communication Breakdown by Modifying the Neuronal Cytoskeleton
title_short The Beta-Amyloid Protein of Alzheimer's Disease: Communication Breakdown by Modifying the Neuronal Cytoskeleton
title_sort beta-amyloid protein of alzheimer's disease: communication breakdown by modifying the neuronal cytoskeleton
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3876695/
https://www.ncbi.nlm.nih.gov/pubmed/24416616
http://dx.doi.org/10.1155/2013/910502
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