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The role of myelin damage in Alzheimer’s disease pathology

Although Alois Alzheimer described myelin disruption in Alzheimer’s disease (AD) as early as in 1911, his observation has escaped the attention of researchers since that time. Alzheimer’s disease has been mainly considered as a grey matter disorder; nevertheless, recent evidence suggests that myelin...

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Detalles Bibliográficos
Autores principales: Papuć, Ewa, Rejdak, Konrad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7069444/
https://www.ncbi.nlm.nih.gov/pubmed/32190145
http://dx.doi.org/10.5114/aoms.2018.76863
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author Papuć, Ewa
Rejdak, Konrad
author_facet Papuć, Ewa
Rejdak, Konrad
author_sort Papuć, Ewa
collection PubMed
description Although Alois Alzheimer described myelin disruption in Alzheimer’s disease (AD) as early as in 1911, his observation has escaped the attention of researchers since that time. Alzheimer’s disease has been mainly considered as a grey matter disorder; nevertheless, recent evidence suggests that myelin impairment may play an important role in AD pathology. Classical neuropathological changes in AD, e.g. the accumulation of aggregated Aβ 42 and the presence of neurofibrillary tangles, are responsible for neuronal loss, but they may also induce death of oligodendrocytes and myelin damage. There is also evidence that myelin pathology may even precede Aβ and tau pathologies in AD. The state of the art does not allow us to determine whether myelin damage is a primary or a secondary injury in AD subjects. The article presents an overview of current knowledge on the role of myelin in AD pathology and its interactions with Aβ and tau pathologies.
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spelling pubmed-70694442020-03-18 The role of myelin damage in Alzheimer’s disease pathology Papuć, Ewa Rejdak, Konrad Arch Med Sci State of the Art Paper Although Alois Alzheimer described myelin disruption in Alzheimer’s disease (AD) as early as in 1911, his observation has escaped the attention of researchers since that time. Alzheimer’s disease has been mainly considered as a grey matter disorder; nevertheless, recent evidence suggests that myelin impairment may play an important role in AD pathology. Classical neuropathological changes in AD, e.g. the accumulation of aggregated Aβ 42 and the presence of neurofibrillary tangles, are responsible for neuronal loss, but they may also induce death of oligodendrocytes and myelin damage. There is also evidence that myelin pathology may even precede Aβ and tau pathologies in AD. The state of the art does not allow us to determine whether myelin damage is a primary or a secondary injury in AD subjects. The article presents an overview of current knowledge on the role of myelin in AD pathology and its interactions with Aβ and tau pathologies. Termedia Publishing House 2018-08-28 /pmc/articles/PMC7069444/ /pubmed/32190145 http://dx.doi.org/10.5114/aoms.2018.76863 Text en Copyright: © 2018 Termedia & Banach http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
spellingShingle State of the Art Paper
Papuć, Ewa
Rejdak, Konrad
The role of myelin damage in Alzheimer’s disease pathology
title The role of myelin damage in Alzheimer’s disease pathology
title_full The role of myelin damage in Alzheimer’s disease pathology
title_fullStr The role of myelin damage in Alzheimer’s disease pathology
title_full_unstemmed The role of myelin damage in Alzheimer’s disease pathology
title_short The role of myelin damage in Alzheimer’s disease pathology
title_sort role of myelin damage in alzheimer’s disease pathology
topic State of the Art Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7069444/
https://www.ncbi.nlm.nih.gov/pubmed/32190145
http://dx.doi.org/10.5114/aoms.2018.76863
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