Peroxisomal defects in microglial cells induce a disease-associated microglial signature
Open accessAbstract
Microglial cells ensure essential roles in brain homeostasis. In pathological condition, microglia adopt a common signature, called disease-associated microglial (DAM) signature, characterized by the loss of homeostatic genes and the induction of disease-associated genes. In X-linked adrenoleukodystrophy (X-ALD), the most common peroxisomal disease, microglial defect has been shown to precede myelin degradation and may actively contribute to the neurodegenerative process. We previously established BV-2 microglial cell models bearing mutations in peroxisomal genes that recapitulate some of the hallmarks of the peroxisomal β-oxidation defects such as very long-chain fatty acid (VLCFA) accumulation. In these cell lines, we used RNA-sequencing and identified large-scale reprogramming for genes involved in lipid metabolism, immune response, cell signaling, lysosome and autophagy, as well as a DAM-like signature. We highlighted cholesterol accumulation in plasma membranes and observed autophagy patterns in the cell mutants. We confirmed the upregulation or downregulation at the protein level for a few selected genes that mostly corroborated our observations and clearly demonstrated increased expression and secretion of DAM proteins in the BV-2 mutant cells. In conclusion, the peroxisomal defects in microglial cells not only impact on VLCFA metabolism but also force microglial cells to adopt a pathological phenotype likely representing a key contributor to the pathogenesis of peroxisomal disorders.
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RNA sequencing revealed large-scale reprogramming of genes involved in lipid metabolism, immune response, cell signaling, and autophagy in ABCD1-mutated microglia.
“RNA sequencing revealed large-scale reprogramming of genes involved in lipid metabolism, immune response, cell signaling, and autophagy [350].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [350]
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Glycoprotein NMB: an Emerging Role in Neurodegenerative Disease
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Self-citationMetabolic rerouting via SCD1 induction impacts X-linked adrenoleukodystrophy
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Inter-domain dynamics drive cholesterol transport by NPC1 and NPC1L1 proteins
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Human mevalonate pyrophosphate decarboxylase is localized in the cytosol
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Molecular Biomarkers for Adrenoleukodystrophy: An Unmet Need
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The Role of Microglia in Inherited White-Matter Disorders and Connections to Frontotemporal Dementia
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Potential Involvement of Peroxisome in Multiple Sclerosis and Alzheimer’s Disease
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Very-Long-Chain Fatty Acids Activate Lysosomal Hydrolases in Neonatal Human Skin Tissue
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Tawbeh, A., Gondcaille, C., Saih, F.-E., Raas, Q., Loichot, D., Hamon, Y., Keime, C., Benani, A., Di Cara, F., Cherkaoui-Malki, M., et al. (2025) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2025.1542938 · Cited by 21 · see citing works
Self-citationImmune response of BV-2 microglial cells is impacted by peroxisomal beta-oxidation
Tawbeh, A., Raas, Q., Tahri-Joutey, M., Keime, C., Kaiser, R., Trompier, D., Nasser, B., Bellanger, E., Dessard, M., Hamon, Y., et al. (2023) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1299314 · Cited by 18 · see citing works
Self-citationABCD1 Transporter Deficiency Results in Altered Cholesterol Homeostasis
Buda, A., Forss-Petter, S., Hua, R., Jaspers, Y., Lassnig, M., Waidhofer-Söllner, P., Kemp, S., Kim, P., Weinhofer, I., & Berger, J. (2023) · Biomolecules · doi:10.3390/biom13091333 · Cited by 14 · see citing works
Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy
Bougnères, P., & Le Stunff, C. (2025) · Genes · doi:10.3390/genes16050590 · Cited by 11 · see citing works
Wang, S., Wang, J., Hu, Z., Wu, L., & Huang, L. (2026) · Experimental Neurology · doi:10.1016/j.expneurol.2026.115663 · Cited by 7 · see citing works
Villoria-González, A., Zierfuss, B., Parzer, P., Heuboeck, E., Zujovic, V., Waidhofer‐Söllner, P., Ponleitner, M., Rommer, P. S., Göpfert, J. C., Forss‐Petter, S., et al. (2023) · Biomolecules · doi:10.3390/biom13121696 · Cited by 6 · see citing works
Sahu, R. K., Yang, Y., & Chung, H.-L. (2026) · iScience · doi:10.1016/j.isci.2026.114724 · Cited by 5 · see citing works
Faverio, P., Rebora, P., Franco, G., Amato, A., Corti, N., Cattaneo, K., Spiti, S., Zanini, U., Maloberti, A., Giannattasio, C., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26125790 · Cited by 5 · see citing works
Self-citationCara, F. D., & Savary, S. (2026) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2026.1745086 · Cited by 3 · see citing works
Self-citationMetabolic Reprogramming of Microglia in Neuroinflammation and Depression
Wu, Q., Tian, J., Gu, Y., Bi, X., & Zhang, H. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27093984 · Cited by 3 · see citing works
Progress in leukodystrophies with zebrafish
Shih, H., Raas, Q., & Bonkowsky, J. L. (2024) · Development Growth & Differentiation · doi:10.1111/dgd.12907 · Cited by 3 · see citing works
Self-citationEberhart, T., Charles, K. N., Salumbides-Torres, B., Price, N., Fliesler, S. J., Faust, P. L., & Kovacs, W. J. (2026) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2026.1636268 · Cited by 1 · see citing works
Cui, Q., Zheng, K., Liu, Q., Wang, L., Liu, Y., Bai, R., Zhang, W., Guo, J., Chang, X., & Wang, J. (2026) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2026.1921079 · Cited by 1 · see citing works
Zellweger Spectrum Disorders: Beyond the Peroxisome
Maheshwari, A., & Huisman, T. A. (2026) · Newborn · doi:10.5005/jp-journals-11002-0164 · Cited by 1 · see citing works
Analytical subcellular fractionation of microglial BV-2 cells with peroxisomal beta-oxidation defect
Tahri-Joutey, M., Hamer, I., Tevel, V., Raas, Q., Gondcaille, C., Trompier, D., Kebbaj, R. E., Ménétrier, F., Latruffe, N., Lizard, G., et al. (2025) · Histochemistry and Cell Biology · doi:10.1007/s00418-025-02372-7 · Cited by 1 · see citing works
Self-citationPeroxisomes in Alzheimer’s disease: emerging mechanistic insights and therapeutic opportunities
Liu, T., Liu, Y., Zhang, Y., Wang, J., Ren, Y., Fu, S., Han, L., 蒋鹏成, Chen, J., Li, Y., et al. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1960320
- Authors
- Raas, Q., Tawbeh, A., Tahri-Joutey, M., Gondcaille, C., Keime, C., Kaiser, R., Trompier, D., Nasser, B., Leoni, V., Bellanger, E., Boussand, M., Hamon, Y., Benani, A., Di Cara, F., Truntzer, C., Cherkaoui-Malki, M., Andreoletti, P., & Savary, S.
- Affiliations
- Université de Bourgogne (FR)
- Centre National de la Recherche Scientifique (FR)
- Université Hassan 1er (MA)
- University of Milano-Bicocca (IT)
- Centre Georges François Leclerc (FR)
- Corresponding author
- Savary, Stéphane
- ORCID
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2023-04-17
- Volume
- 16
- Issue
- Sec. Brain Disease Mechanisms
- Pages
- 1170313-1170313
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC10149961
- OpenAlex
- W4366216678
- Cited by
- 16
- References
- 151
- Citations by year
- 2026: 8 · 2025: 4 · 2024: 1 · 2023: 3
- FWCI
- 1.65
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- BOA (University of Milano-Bicocca) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Greater South Information System
- Funders
- Agence Nationale de la Recherche (ANR-10-INBS-0009, ANR-17-CE15-0032)
- Université de Namur
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
- Health Sciences › Medicine › Physiology › Lysosomal Storage Disorders Research
- Keywords
- microglia, peroxisomal disorders, X-linked adrenoleukodystrophy, very long chain fatty acids, BV-2 cells, microglial reprogramming, cholesterol accumulation, autophagy, lysosomes, lipid metabolism, neurodegeneration, myelin degradation
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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.
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