Enhancing myelin renewal reverses cognitive dysfunction in a murine model of Alzheimer’s disease
Open accessAbstract
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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Nearly all studies of oligodendrocytes and myelin in amyloid mouse models of AD have focused on the effect of amyloid plaques and Aβ on oligodendrocytes and myelin, partially describing secondary demyelination or hypomyelination.
“Nearly all have focused on the effect of amyloid plaques and Aβ on oligodendrocytes and myelin, partially describing secondary demyelination or hypomyelination.”
From Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease (2023) · cites this paper as [20]
The Introduction (page unavailable) reports that Aβ deposition causes focal demyelination and changes in oligodendrocyte precursor cells in AD mouse models. It does not establish that nearly all prior studies focused on plaque or Aβ effects, or characterize their findings as secondary hypomyelination. (LLM, conf=0.82)
Experimental — accuracy not yet measuredOnly a few studies have experimentally investigated oligodendrocytes and myelin in amyloid mouse models of AD.
“Only a few studies have experimentally investigated oligodendrocytes and myelin in amyloid mouse models of AD20,21,41–43.”
From Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease (2023) · cites this paper as [20]
Myelin alterations have been implicated in Alzheimer's disease.
“myelin alterations have been implicated in AD7–9”
From Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice (2024) · cites this paper as [7]
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- 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
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2021-07
- Volume
- 109
- Issue
- 14
- Pages
- 2292-2307.e5
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC8298291
- OpenAlex
- W3169884592
- Cited by
- 346
- References
- 71
- Citations by year
- 2026: 55 · 2025: 75 · 2024: 70 · 2023: 75 · 2022: 52 · 2021: 17 · 2020: 1 · 2012: 1
- 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
- Health Sciences › Medicine › Physiology › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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