Lipid metabolism transcriptomics of murine microglia in Alzheimer’s disease and neuroinflammation
Open accessAbstract
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid-β (Aβ) plaques followed by intracellular neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau. An unrestrained immune response by microglia, the resident cells of the central nervous system (CNS), leads to neuroinflammation which can amplify AD pathology. AD pathology is also driven by metabolic dysfunction with strong correlations between dementia and metabolic disorders such as diabetes, hypercholesterolemia, and hypertriglyceridemia. Since elevated cholesterol and triglyceride levels appear to be a major risk factor for developing AD, we investigated the lipid metabolism transcriptome in an AD versus non-AD state using RNA-sequencing (RNA-seq) and microarray datasets from N9 cells and murine microglia. We identified 52 differentially expressed genes (DEG) linked to lipid metabolism in LPS-stimulated N9 microglia versus unstimulated control cells using RNA-seq, 86 lipid metabolism DEG in 5XFAD versus wild-type mice by microarray, with 16 DEG common between both datasets. Functional enrichment and network analyses identified several biological processes and molecular functions, such as cholesterol homeostasis, insulin signaling, and triglyceride metabolism. Furthermore, therapeutic drugs targeting lipid metabolism DEG found in our study were identified. Focusing on drugs that target genes associated with lipid metabolism and neuroinflammation could provide new targets for AD drug development.
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Metabolites such as lipid, free fatty acid, and glucose are capable of stimulating microglia and metabolic reprogramming has inherent linkage with microglial activation.
“Recently, acuumulating evidence show that metabolites such as lipid, free fatty acid, and glucose are capable of stimulating microglia and metabolic reprogramming has inherent linkage with microglial activation (immunobolism) [17–20].”
From HIV-TAT dysregulates microglial lipid metabolism through SREBP2/miR-124 axis: Implication of lipid droplet accumulation microglia in NeuroHIV (2025) · cites this paper as [18]
The Introduction links increased microglial lipid metabolism to the energy needed for activation, and the Discussion describes lipids as a fuel source for activated microglia. Neither passage establishes that lipids, free fatty acids, or glucose stimulate microglia; the paper supports a link between lipid metabolism and activation, but not the full list of proposed stimuli. Page numbers were not provided in our copy. (LLM, conf=0.85)
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Cognitive impairments in prediabetes and diabetes: From pathogenesis to comprehensive therapy
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- Authors
- Shippy, D. C., & Ulland, T. K.
- Affiliations
- University of Wisconsin–Madison (US)
- Corresponding author
- Ulland, Tyler K.
- ORCID
- Ulland, Tyler K.
- Venue
- Scientific Reports
- Published
- 2023-09-08
- Volume
- 13
- Issue
- 1
- Pages
- 14800-14800
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC10491618
- OpenAlex
- W4386543809
- Cited by
- 35
- References
- 72
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 13 · 2023: 2
- FWCI
- 3.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- National Institute on Aging (R21AG068652, R01AG037639, R01AG070973, R01AG083883)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, microglia, lipid metabolism, neuroinflammation, transcriptome, cholesterol homeostasis, insulin signaling, triglyceride metabolism, amyloid-beta, tau protein, 5xFAD mice, lipopolysaccharide stimulation, N9 cells, therapeutic target, metabolic dysfunction
- MeSH terms
- Neuroinflammatory Diseases, Alzheimer Disease, Animals, Hypercholesterolemia, Triglycerides, Microglia, Lipid Metabolism, Mice, Transcriptome
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