A shared disease-associated oligodendrocyte signature among multiple CNS pathologies
Open accessAbstract
Alzheimer's disease (AD) is a complex neurodegenerative disease, perturbing neuronal and non-neuronal cell populations. In this study, using single-cell transcriptomics, we mapped all non-immune, non-neuronal cell populations in wild-type and AD model (5xFAD) mouse brains. We identified an oligodendrocyte state that increased in association with brain pathology, which we termed disease-associated oligodendrocytes (DOLs). In a murine model of amyloidosis, DOLs appear long after plaque accumulation, and amyloid-beta (Aβ) alone was not sufficient to induce the DOL signature in vitro. DOLs could be identified in a mouse model of tauopathy and in other murine neurodegenerative and autoimmune inflammatory conditions, suggesting a common response to severe pathological conditions. Using quantitative spatial analysis of mouse and postmortem human brain tissues, we found that oligodendrocytes expressing a key DOL marker (SERPINA3N/SERPINA3 accordingly) are present in the cortex in areas of brain damage and are enriched near Aβ plaques. In postmortem human brain tissue, the expression level of this marker correlated with cognitive decline. Altogether, this study uncovers a shared signature of oligodendrocytes in central nervous system pathologies.
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Pro-inflammatory DAM and DAO localize to Aβ plaques.
“The localization of pro‐inflammatory DAM and DAO to Aβ plaques 16 , 17 , 46 further reinforces the role of Aβ as the primary trigger for these immune responses.”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [46]
The Results section on spatial analysis reports that disease-associated oligodendrocytes (called DOLs in this paper) are enriched near Aβ plaques in 5xFAD mice. The paper identifies DAM, but the cited passages do not establish that DAM localize to plaques or characterize both cell states as pro-inflammatory. Its Discussion also cautions that Aβ alone is not sufficient to induce the DOL state. (LLM, conf=0.84)
Experimental — accuracy not yet measuredLike DAM, which appears in 5XFAD at 1 to 2 months of age, DAO is also enriched near Aβ plaques at 9 to 10 months of age.
“Like DAM, which appears in 5XFAD at 1 to 2 months of age, DAO is also enriched near Aβ plaques at 9 to 10 months of age. 17 , 46”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [46]
The Results section on identifying disease-associated oligodendrocytes says DAM appear in 5xFAD mice at 1–2 months and the oligodendrocyte state, called DOLs in this paper, is detected around 9–10 months. The spatial-analysis Results show these cells near Aβ plaques, but that analysis used 16-month-old mice; it does not establish plaque proximity specifically at 9–10 months. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSingle cell RNA-seq analysis of mouse models of AD demonstrated signature alterations in oligodendrocytes, specifically nearby amyloid plaques.
“Similarly, single cell RNA-seq analysis of mouse models of AD demonstrated signature alterations in oligodendrocytes, specifically nearby amyloid plaques44,45.”
From Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease (2023) · cites this paper as [45]
O_3 cluster was distinctly enriched for marker genes of disease-associated oligodendrocytes (DAO) compared to other oligodendrocyte clusters, with DAO signature most prominently expressed in 5XFAD;PS19.
“Moreover, the O_3 cluster was distinctly enriched for marker genes of disease‐associated oligodendrocytes (DAO) 17 , 46 compared to other oligodendrocyte clusters, with the DAO signature most prominently expressed in the 5XFAD;PS19 model (Figure S4A,B in supporting information).”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [46]
Some DE genes recently identified as markers of DAOs in AD mouse models were also upregulated in cluster 9 versus cluster 2, such as H2-D1, Il33 and C4b.
“Some DE genes recently identified as markers of DAOs in AD mouse models61 were also upregulated in cluster 9 versus cluster 2, such as those mediating the inflammatory process (H2-D1, Il33 and C4b)”
From The APOE-R136S mutation protects against APOE4-driven tau pathology, neurodegeneration, and neuroinflammation (2023) · cites this paper as [61]
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van den Bosch, A. M. R., Khoo, J. H., Lu, Z., Liang, H., Wever, D., Pu, L., Eggen, B. J. L., Uhlén, M., Smolders, J., Hamann, J., et al. (2026) · Cell Reports · doi:10.1016/j.celrep.2026.117538 · Cited by 6 · see citing works
TGFβ signaling mediates microglial resilience to spatiotemporally restricted myelin degeneration
Zhu, K., Liu, Y., Min, J.-H., Joshua, V., Lin, J., Li, Y., Kreutzmann, J. C., Guo, Y., Xia, W., Mohammadi, E., et al. (2026) · Nature Neuroscience · doi:10.1038/s41593-025-02161-4 · Cited by 11 · see citing works
ApoE expression across the CNS: Who, What, Where, When, and How (much)?
Nolt, G. L., Lucido, C. C., Smith, L. M., & Johnson, L. A. (2026) · Molecular Neurodegeneration Advances · doi:10.1186/s44477-026-00028-x · Cited by 2 · see citing works
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Human brain microRNAs exhibit cell-type specificity and age dependence
Dubnov, S., Laski, L., Zchut, I., Avidan, O., Bennett, E. R., Greenberg, D. S., Turjeman, A., Nitzan, M., Paldor, I., & Soreq, H. (2026) · doi:10.64898/2026.01.04.697535
- Authors
- Kenigsbuch, M., Bost, P., Halevi, S., Chang, Y., Chen, S., Ma, Q., Hajbi, R., Schwikowski, B., Bodenmiller, B., Fu, H., Schwartz, M., & Amit, I.
- Affiliations
- Weizmann Institute of Science (IL)
- Centre National de la Recherche Scientifique (FR)
- The Ohio State University (US)
- University of Zurich (CH)
- Corresponding author
- Schwartz, Michal
- Amit, Ido
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2022-06-27
- Volume
- 25
- Issue
- 7
- Pages
- 876-886
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC9724210
- OpenAlex
- W4283712086
- Cited by
- 233
- References
- 63
- Citations by year
- 2026: 48 · 2025: 54 · 2024: 65 · 2023: 52 · 2022: 14
- FWCI
- 31.58
- Type
- journal article
- Language
- en
- Update notices
- correction (2023-01-31)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (1r56ag066782-01)
- National Institute on Aging (R56 AG066782, K01AG056673)
- National Institute of General Medical Sciences (R01GM131399)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Single-cell and spatial transcriptomics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- oligodendrocytes, Alzheimer's disease, amyloid plaques, amyloidosis, tauopathy, 5xFAD mice, Serpina3n, cognitive decline, neuroinflammation, central nervous system pathology, single-cell transcriptomics
- MeSH terms
- Alzheimer Disease, Animals, Brain, Disease Models, Animal, Humans, Mice, Transgenic, Oligodendroglia, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Neurodegenerative Diseases, Mice, Plaque, Amyloid
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