Cited by 346Alzheimer's disease research and treatmentsNeurogenesis and neuroplasticity mechanismsNeuroinflammation and Neurodegeneration Mechanisms

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Enhancing myelin renewal reverses cognitive dysfunction in a murine model of Alzheimer’s disease

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Chen, Jing-Fei, Liu, Kun, Hu, Bo, Li, Rong-Rong, Xin, Wendy, Chen, Hao, Wang, Fei, Chen, Lin, Li, Rui-Xue, Ren, Shu-Yu, Xiao, Lan, Chan, Jonah R., Mei, Feng·2021·Neuron

DOI 10.1016/j.neuron.2021.05.012PMC PMC8298291

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Abstract

Severe cognitive decline is a hallmark of Alzheimer's disease (AD). In addition to gray matter loss, significant white matter pathology has been identified in AD patients. Here, we characterized the dynamics of myelin generation and loss in the APP/PS1 mouse model of AD. Unexpectedly, we observed a dramatic increase in the rate of new myelin formation in APP/PS1 mice, reminiscent of the robust oligodendroglial response to demyelination. Despite this increase, overall levels of myelination are decreased in the cortex and hippocampus of APP/PS1 mice and postmortem AD tissue. Genetically or pharmacologically enhancing myelin renewal, by oligodendroglial deletion of the muscarinic M1 receptor or systemic administration of the pro-myelinating drug clemastine, improved the performance of APP/PS1 mice in memory-related tasks and increased hippocampal sharp wave ripples. Taken together, these results demonstrate the potential of enhancing myelination as a therapeutic strategy to alleviate AD-related cognitive impairment.

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Additional file 3 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622301
Additional file 4 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622304
Additional file 5 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622307
Additional file 6 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622310
Additional file 1 of Maternal immune suppression during pregnancy does not prevent abnormal behavior in offspring
Griffin, A., Bowles, T., Solis, L., Railey, T., Beauti, S., Robinson, R., Spencer, S.-K., Shaffery, J. P., & Wallace, K. L. (2024) · Figshare · doi:10.6084/m9.figshare.26698310
Additional file 2 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622298
Additional file 1 of Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Wang, N., Wang, M., Jeevaratnam, S., Rosenberg, C. L., Ikezu, T. C., Shue, F., Doss, S. V., Alnobani, A., Martens, Y. A., Wren, M. C., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21622295

Authors: Chen, J.-F., Liu, K., Hu, B., Li, R.-R., Xin, W., Chen, H., Wang, F., Chen, L., Li, R.-X., Ren, S.-Y., Xiao, L., Chan, J. R., & Mei, F.
Affiliations: Army Medical University (CN)
University of California, San Francisco (US)
Corresponding author: Xiao, Lan
Chan, Jonah R.
Mei, Feng
ORCID: Liu, Kun
Hu, Bo
Xin, Wendy
Chen, Hao
Wang, Fei
Chen, Lin
Xiao, Lan
Chan, Jonah R.
Mei, Feng
Venue: Neuron
Publisher: Elsevier BV
Published: 2021-07
Volume: 109
Issue: 14
Pages: 2292-2307.e5
ISSN: 0896-6273 (ISSN-L)
DOI: 10.1016/j.neuron.2021.05.012
PMC: PMC8298291
OpenAlex: W3169884592
Cited by: 346
References: 71
Citations by year: 2026: 55 · 2025: 75 · 2024: 70 · 2023: 75 · 2022: 52 · 2021: 17
FWCI: 33.58
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 385 d)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
Locations: Neuron (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
eScholarship (California Digital Library) (submittedVersion)
Funders: Chongqing Science and Technology Commission
Doctor Miriam and Sheldon G Adelson Medical Research Foundation
National Institutes of Health
Chongqing Municipal Education Commission
National Institute of Neurological Disorders and Stroke
National Natural Science Foundation of China
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: Alzheimer's disease, myelination, white matter pathology, APP/PS1 mice, oligodendrocytes, demyelination, M1 muscarinic receptor, clemastine, cognitive impairment, memory, hippocampal ripples, treatment options
MeSH terms: Alzheimer Disease, Animals, Cerebral Cortex, Disease Models, Animal, Mice, Transgenic, Myelin Sheath, Amyloid beta-Protein Precursor, Maze Learning, Mice, Presenilin-1, Cognitive Dysfunction

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Enhancing myelin renewal reverses cognitive dysfunction in a murine model of Alzheimer’s disease

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