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White matter damage in Alzheimer’s disease: contribution of oligodendrocytes

Zhou, Jinyu, Zhang, Peng, Zhang, Bo, Kong, Yuhan·2022·Current Alzheimer Research
DOI 10.2174/1567205020666221021115321PMC PMC9982194
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Abstract

Alzheimer’s disease (AD) is an age-related neurodegenerative disease seriously influencing the quality of life and is a global health problem. Many factors affect the onset and development of AD, but specific mechanisms underlying the disease are unclear. Most studies investigating AD have focused on neurons and the gray matter in the central nervous system (CNS) but have not led to effective treatments. Recently, an increasing number of studies have focused on white matter (WM). Magnetic resonance imaging and pathology studies have shown different degrees of WM abnormality during the progression of AD. Myelin sheaths, the main component of WM in the CNS, wrap and insulate axons to ensure conduction of the rapid action potential and axonal integrity. WM damage is characterized by progressive degeneration of axons, oligodendrocytes (OLs), and myelin in one or more areas of the CNS. The contributions of OLs to AD progression have, until recently, been largely overlooked. OLs are integral to myelin production, and the proliferation and differentiation of OLs, an early characteristic of AD, provide a promising target for preclinical diagnosis and treatment. However, despite some progress, the key mechanisms underlying the contributions of OLs to AD remain unclear. Given the heavy burden of medical treatment, a better understanding of the pathophysiological mechanisms underlying AD is vital. This review comprehensively summarizes the results on WM abnormalities in AD and explores the relationship between OL progenitor cells and the pathogenesis of AD. Finally, the underlying molecular mechanisms and potential future research directions are discussed.

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  • In AD, intercellular networks become maladaptive, leading to sustained inflammation, impaired synaptic support, defective myelination, and breakdown of the blood-brain barrier, ultimately amplifying neurodegeneration.

    “In AD, these networks become maladaptive, leading to sustained inflammation, impaired synaptic support, defective myelination (Nasrabady et al.; 2018, Zhou et al., 2022), and breakdown of the blood-brain barrier (BBB), ultimately amplifying neurodegeneration (Heneka et al., 2015; Sweeney et al., 2018).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Zhou et al., 2022

  • Oligodendrocyte lineage cells display impaired myelin maintenance and white-matter abnormalities, increasingly recognized as important contributors to cognitive decline in AD.

    “Oligodendrocyte lineage cells display impaired myelin maintenance and white-matter abnormalities, increasingly recognized as important contributors to cognitive decline in AD (Nasrabady et al., 2018; Zhou et al., 2022).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Zhou et al., 2022

  • AD is consistently associated with white-matter abnormalities and demyelination, contributing to cognitive and structural decline.

    “The disease is consistently associated with white-matter abnormalities and demyelination, contributing to cognitive and structural decline (Nasrabady et al., 2018; Zhou et al., 2022; Zovoilis et al., 2011).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Zhou et al., 2022

  • OLs and OPCs are vulnerable to Aβ toxicity, oxidative stress, and inflammation, leading to impaired myelination and OL death.

    “OLs and their precursor cells (OPCs) are vulnerable to Aβ toxicity, oxidative stress, and inflammation, leading to impaired myelination and OL death (Nasrabady et al., 2018; Wei et al., 2020; Zhou et al., 2022).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Zhou et al., 2022

  • Converging transcriptomic studies consistently report dysregulation of myelin-regulatory pathways in AD white matter.

    “While direct AD-specific data for miR-23a/b remain limited, converging transcriptomic studies consistently report dysregulation of myelin-regulatory pathways in AD white matter, suggesting indirect relevance within OL-mediated degeneration (Nasrabady et al., 2018; Lin et al., 2013; Zhou et al., 2022).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Zhou et al., 2022

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Sorted by citations

Authors
Zhou, J., Zhang, P., Zhang, B., & Kong, Y.
Affiliations
  • Department of Rehabilitation Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing- 400042, China
  • Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing- 400010, China
  • Department of Basic Medicine, Chongqing Medical and Pharmaceutical College, Chongqing- 401331, China
ORCID
Zhou, Jinyu
Venue
Current Alzheimer Research
Publisher
Bentham Science Publishers Ltd.
Published
2022-08
Volume
19
Issue
9
Pages
629-640
ISSN
1567-2050
DOI
10.2174/1567205020666221021115321
PMC
PMC9982194
Cited by
18
References
14
Language
en
Licence
creativecommons.org/licenses/by/4.0/legalcode (unspecified)
Funders
  • National Natural Science Foundation of China (81401865)
  • Natural Science Foundation of Chongqing Science and Technology Bureau (cstc2019jcyjmsxmX0339)

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