Multi-omics reveals changes in astrocyte fatty acid metabolism during early stages of Alzheimer's disease
Open accessAbstract
BACKGROUND: Although astrocytes are known to contribute to Alzheimer's disease (AD) progression, their dynamic molecular alterations remain poorly characterized, particularly in early stages of the disease. METHODS: We performed multi-omics profiling (transcriptomics, proteomics, spatial metabolomics) of astrocytes from APP/PS1 and WT mice to characterize dynamic changes during AD progression. To assess similar changes in early human AD, we analyzed single-nucleus RNA sequencing data from human samples. RESULTS: Transcriptomic analysis of astrocytes from APP/PS1 and WT mice at five time points (2, 4, 6, 9, and 12 months of age) showed notable gene expression differences at 6 months, with reduced activity in fatty acid metabolism pathways (e.g., PPAR signaling, biosynthesis of unsaturated fatty acids). An astrocyte-specific metabolic model confirmed these disruptions. Proteomic analysis corroborated this by showing decreased activity in pathways like butanoate metabolism and PPAR signaling. Spatial metabolomics of brain slices from APP/PS1 and WT mice highlighted fatty acid enrichment in the hippocampus and cortex, alongside differential metabolites specific to the AD mouse model. Single-cell RNA sequencing analysis of human brain samples further showed fatty acid metabolism abnormalities in astrocytes from early AD cases versus controls, emphasizing its role in AD progression. CONCLUSION: Our study identified abnormal fatty acid metabolism as an early feature of astrocytes in AD, suggesting an association between dysregulated fatty acid metabolism and disease progression.
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Astrocytic lipid metabolism pathways are downregulated in the APP/PS1 amyloidosis model.
“This finding aligns with reports that astrocytic lipid metabolism pathways are downregulated in the APP/PS1 amyloidosis model. 52”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [52]
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Upaganlawar, A. B., Upasani, C. D., & Ihim, S. A. (2022) · Springer eBooks · doi:10.1007/978-981-16-7606-2_14 · Cited by 2 · see citing works
National Health and Nutrition Examination Survey (NHANES), 2003-2004: Version 6
(2010) · ICPSR Data Holdings · doi:10.3886/icpsr25503.v6
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Astrocytic lipid dysregulation as an early driver of neurodegeneration
Kim, W. S., & Halliday, G. M. (2026) · Nature Reviews Neurology · doi:10.1038/s41582-026-01238-3 · Cited by 5 · see citing works
Liu, Y., Fu, R., Ge, C., Long, Z., Wang, H., & He, G. (2026) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2026.111994 · Cited by 1 · see citing works
Park, J. H., Kim, B., Al‐Amin, M. M., Tate, M. D., Sharify, A. D., John, S. K., Karahan, H., Lu, H., Dabin, L. C., & Kim, J. (2026) · Alzheimer's & Dementia · doi:10.1002/alz.71742
“52 53–55 In contrast, the immune module (Mod6) was upregulated in both 5XFAD and 5XFAD;PS19 but not in PS19 (Figure 2D–”
- Authors
- Zhong, J., Li, M., Dai, Z., & Wan, J.
- Affiliations
- Hong Kong University of Science and Technology (HK)
- Southern University of Science and Technology (CN)
- Peking University (CN)
- Corresponding author
- Dai, Ziwei
- Wan, Jun
- Venue
- Neurochemistry International
- Publisher
- Elsevier BV
- Published
- 2025-11
- Volume
- 190
- Pages
- 106049
- ISSN
- 0197-0186 (ISSN-L)
- OpenAlex
- W4413840496
- Cited by
- 3
- References
- 89
- Citations by year
- 2026: 3
- FWCI
- 1.94
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neurochemistry International (publishedVersion, cc-by-nc-nd)
- Research Square (acceptedVersion, cc-by)
- PubMed (publishedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- Shenzhen Technology Development Program (JCYJ20220818100215033)
- Guangxi Natural Science Foundation (2020GXNSFDA238009)
- National Natural Science Foundation of China (82071586, 12371489)
- National Key Research and Development Program of China (2021YFF1201000)
- Guangdong Innovative and Entrepreneurial Research Team Program (2021ZT09Y104)
- Southern University of Science and Technology
- Defense Health Agency
- Amazon Research Awards
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, astrocytes, fatty acid metabolism, early-stage disease, APP/PS1 mice, PPAR signaling, unsaturated fatty acid biosynthesis, butanoate metabolism, hippocampus, cortex, single-nucleus RNA sequencing, multi-omics
- MeSH terms
- Multiomics, Alzheimer Disease, Animals, Astrocytes, Fatty Acids, Female, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Proteomics, Mice, Metabolomics, Transcriptome
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.
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