alexa Does Myelin Play the Leading Role in Alzheimerâ€
ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
Open Access

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Commentary

Does Myelin Play the Leading Role in Alzheimer’s Disease Pathology?

Ewa Papuć1* and Konrad Rejdak1,2

1Department of Neurology of Medical University of Lublin, Poland

2Medical Research Center, Polish Academy of Sciences, Warsaw, Poland

*Corresponding Author:
Ewa Papuć
Department of Neurology
Medical University of Lublin
Jaczewskiego Str, 20-954, Lublin, Poland
Tel: +48-81-7244-720
E-mail: [email protected]

Received date: April 12, 2017; Accepted date: April 26, 2017; Published date: April 30, 2017

Citation: Papuć E, Rejdak K (2017) Does Myelin Play the Leading Role in Alzheimer’s Disease Pathology? J Alzheimers Dis Parkinsonism 7:321. doi:10.4172/2161-0460.1000321

Copyright: © 2017 Papuć E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Although Alzheimer’s disease (AD) has been mainly considered as a grey matter disorder, there is emerging evidence that myelin impairment may play an important role in AD pathology. These data come from animal neuropathological studies, but also from human pathological, biochemical and brain MRI studies. Classical neuropathological changes in AD such as the accumulation of aggregated Aß 42 and the presence of neurofibrillary tangles are responsible for neuronall loss, but they may also induce death of oligodendrocytes and myelin impairment. Accelerated deposition of Aß in brains of AD patients induces damage to oligodendrocytes and results in impaired myelin production. What is more interesting, there is also evidence that myelin pathology may precede Aß and tau pathologies in AD. Recent studies suggest that Aß and tau proteins may be by-products of myelin repair in AD, instead of being the primary underlying cause of dementia. This seems possible, considering the fact that attempts to control clinical symtomps of AD by removing Aß from the human brain have been unsuccesful. In this article, current knowledge on the place of myelin in AD pathology and its interactions with Aß and tau pathology is reviewed.

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