Inefficient clearance of myelin debris by microglia impairs remyelinating processes
Open accessAbstract
An imbalance between remyelinating and demyelinating rates underlies degenerative processes in demyelinating diseases such as multiple sclerosis. An optimal therapeutic strategy would be to stimulate remyelination while limiting demyelination. Although accumulation of myelin debris impairs remyelination, the mechanisms regulating the clearance of such debris by mononuclear phagocytic cells are poorly understood. We demonstrate that after cuprizone intoxication, CCR2-dependent infiltration of mouse bone marrow-derived cells is abundant in demyelinating areas, but that these cells do not impact demyelination. However, in CX3CR1-deficient mice, the clearance of myelin debris by microglia was blocked greatly, affecting the integrity of the axon and myelin sheaths and thus preventing proper remyelination. These results highlight the crucial role played by CX3CR1 in myelin removal and show that there can be no efficient remyelination after a primary demyelinating insult if myelin clearance by microglia is impaired.
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Microglia are critically involved in ensuring the proper containment and removal of neurotoxic material in neurodegenerative disease pathogenesis.
“Mounting evidence suggests that microglia, which are the professional phagocytes of the CNS, are critically involved in ensuring the proper containment and removal of neurotoxic material in neurodegenerative disease pathogenesis (Condello et al., 2015; Hickman et al., 2018; Lampron et al., 2015).”
From SYK coordinates neuroprotective microglial responses in neurodegenerative disease (2022) · cites this paper as Lampron et al., 2015
The Discussion (page not provided) says microglia must clear degenerate myelin from affected axons for efficient remyelination, supporting their importance in debris removal. The paper addresses demyelinating disease specifically; it does not establish a general role in containing neurotoxic material across neurodegenerative diseases. (LLM, conf=0.84)
Experimental — accuracy not yet measuredClearance of myelin debris is believed to be crucial for remyelination and recovery.
“Cessation of cuprizone leads to subsequent remyelination, and clearance of myelin debris is believed to be crucial for remyelination and recovery [5,6].”
From Multifaceted response of microglia in the cuprizone model of demyelination (2026) · cites this paper as [5]
The Discussion reports that impaired microglial clearance left myelin debris in place and led to inefficient remyelination, supporting the remyelination part of the claim. It says that the long-term consequences for neurological deficits remain to be studied, so recovery beyond remyelination is not established by this paper. (LLM, conf=0.83)
Experimental — accuracy not yet measuredMicroglia clear myelin debris and secrete trophic factors to promote oligodendrocyte growth and survival.
“Microglia also clear myelin debris, and secrete trophic factors to promote oligodendrocyte growth and survival [5,11,12].”
From Multifaceted response of microglia in the cuprizone model of demyelination (2026) · cites this paper as [5]
The Abstract and Discussion (page unavailable) support microglial clearance of myelin debris, and the Results link impaired clearance with reduced oligodendrocyte precursor recruitment and proliferation. The Results also report reduced IGF-1 staining, but our copy does not establish that microglia secrete trophic factors to promote oligodendrocyte growth and survival. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMicroglial clearance of myelin debris continues following cuprizone withdrawal.
“indicating that microglial clearance of myelin debris continues following cuprizone withdrawal, as reported in previous studies [3,5].”
From Multifaceted response of microglia in the cuprizone model of demyelination (2026) · cites this paper as [5]
The Results (‘Aberrant myelin patterns in CX3CR1−/− mice’; page unavailable) describe myelin debris inside microglia after 3 and 5 weeks of cuprizone treatment. The paper then examines remyelination after withdrawal, but the passages do not establish that microglia continue clearing debris after withdrawal. The timing asserted in the claim is therefore unsupported. (LLM, conf=0.83)
Experimental — accuracy not yet measuredAccumulation of debris within lesions inhibits oligodendrocyte recruitment and differentiation and delays recovery/remyelination.
“Accumulation of debris within lesions has been demonstrated to inhibit oligodendrocyte recruitment and differentiation (18, 41, 44) and, thus, delay recovery/remyelination.”
From Microglia depletion exacerbates demyelination and impairs remyelination in a neurotropic coronavirus infection (2020) · cites this paper as [44]
The Results (page not provided) report deficient oligodendrocyte precursor cell recruitment in CX3CR1-deficient mice. The Discussion says myelin debris inhibits precursor differentiation, citing earlier work, and links impaired clearance to aberrant remyelination. It does not demonstrate delayed remyelination: staining showed remyelination at a similar extent to wild-type mice. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Efficient myelin debris removal and clearance by phagocytic cells are critical to eliminate inhibitory signals interfering with OPC activation, recruitment to the site of demyelination and/or differentiation into myelinating mature oligodendrocytes.
“Efficient myelin debris removal and clearance by phagocytic cells are critical to eliminate inhibitory signals interfering with OPC activation, recruitment to the site of demyelination and/or differentiation into myelinating mature OLs [14, 26, 27].”
From TREM2 activation on microglia promotes myelin debris clearance and remyelination in a model of multiple sclerosis (2020) · cites this paper as [27]
Recruited cell populations included monocytes and lymphocytes.
“Recruited cell populations included monocytes and lymphocytes.”
From Cuprizone‐induced demyelination triggers a <scp>CD8</scp>‐pronounced T cell recruitment (2021) · cites this paper as Lampron et al., 2015
Lampron and colleagues demonstrated a significant infiltration of transplanted GFP-expressing bone-marrow cells into the CNS, with a peak of infiltration at weeks 4 and 5 of intoxication.
“In line with our observation, Lampron and colleagues demonstrated a significant infiltration of transplanted GFP-expressing bone-marrow cells into the CNS, with a peak of infiltration at weeks 4 and 5 of intoxication (Lampron et al., 2015).”
From Cuprizone‐induced demyelination triggers a <scp>CD8</scp>‐pronounced T cell recruitment (2021) · cites this paper as Lampron et al., 2015
When CCR2-/- instead of CCR2+/+ bone-marrow cells were transplanted, infiltration into the CNS was almost completely blocked without affecting the extent of cuprizone-induced demyelination.
“When CCR2 -/-instead of CCR2 +/+ bone-marrow cells were transplanted, infiltration into the CNS was almost completely blocked without affecting the extent of cuprizoneinduced demyelination.”
From Cuprizone‐induced demyelination triggers a <scp>CD8</scp>‐pronounced T cell recruitment (2021) · cites this paper as Lampron et al., 2015
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“These results differ from previous studies that reported modest (McMahon, Suzuki, & Matsushima, 2002) or significant (Lampron et al., 2015) numbers of macrophages in the CUP model; in the latter case, peripheral macrophage infiltration was CCR2-dependent but did not impact the extent of…”
ResultThe physiology of foamy phagocytes in multiple sclerosis
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- Authors
- Lampron, A., Larochelle, A., Laflamme, N., Préfontaine, P., Plante, M.-M., Sánchez, M. G., Yong, V. W., Stys, P. K., Tremblay, M.-È., & Rivest, S.
- Affiliations
- Université Laval (CA)
- University of Calgary (CA)
- Corresponding author
- Rivest, Serge
- ORCID
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2015-03-16
- Volume
- 212
- Issue
- 4
- Pages
- 481-495
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC4387282
- OpenAlex
- W2096423240
- Cited by
- 595
- References
- 77
- Citations by year
- 2026: 45 · 2025: 42 · 2024: 46 · 2023: 78 · 2022: 86 · 2021: 55 · 2020: 60 · 2019: 61 · 2018: 44 · 2017: 38 · 2016: 29 · 2015: 11
- FWCI
- 32.27
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- remyelination, myelin debris clearance, microglia, CX3CR1, CCR2, demyelination, multiple sclerosis, cuprizone, bone marrow-derived cells, axon integrity
- MeSH terms
- CX3C Chemokine Receptor 1, Animals, Axons, Bone Marrow Cells, Demyelinating Diseases, Myelin Sheath, Phagocytes, Microglia, Mice, Knockout, Receptors, Chemokine, Mice, Receptors, CCR2
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