ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2023
The ketone body β-hydroxybutyrate shifts microglial metabolism and suppresses amyloid-β oligomer-induced inflammation in human microglia.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
- Trial
- Metabolic reprogramming of microglia: Effects on development, disease, and therapeutic potential.Neural regeneration research · 2026Article
- Dietary Patterns, Micronutrient Adequacy, and Metabolic Vulnerability in Alzheimer's Disease: A Critical Narrative Review.Nutrients · 2026Review
- β-hydroxybutyrate regulates microglia M1/M2 polarization and phagocytosis through the JAK1/STAT1 pathway to reduce neuroinflammation and exert anti-epileptic effects.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Unveiling the role of CB2 receptor in beta-hydroxybutyrate mediated modulation of.Journal of physiology and biochemistry · 2026Article
- β-Hydroxybutyrate Exposure is Associated with Increased THCellular and molecular neurobiology · 2026Article
- A ketogenic diet improves memory in females in the APOE4 mouse model of Alzheimer's disease.GeroScience · 2026Article
- The value of targeting ketone body metabolism in inflammatory and autoimmune diseases.Journal of translational medicine · 2026Review
- Article
- Microglia Mitochondrial Metabolism in Neurological Diseases.Molecular neurobiology · 2026Review
- Endogenous β-hydroxybutyrate and the risk of cognitive decline: a nested case-control study in the UK Biobank cohort.Frontiers in aging neuroscience · 2026Article
- Nutritional substrates and microglial metabolic fitness in brain aging and Alzheimer's disease: from lipid handling to TREM2-linked translation.Frontiers in nutrition · 2026Review
- Ketogenic therapy as a potential novel treatment approach for PTSD: an integrative review and proposed mechanistic model.Frontiers in psychiatry · 2026Review
- The role of fatty acids in neurodegenerative diseases: mechanistic insights and therapeutic strategies.Journal of lipid research · 2025Review
- "Rewiring brain immunity: targeting microglial metabolism for neuroprotection in neurodegenerative disorders".Metabolic brain disease · 2025Review
- Gut-specific histamine 3 receptor signaling orchestrates microglia-dependent resolution of peripheral inflammation.The Journal of clinical investigation · 2025Article
- Ketogenic Diet Modulates Gut Microbiota-Brain Metabolite Axis in a Sex- and Genotype-Specific Manner in APOE4 Mice.Journal of neurochemistry · 2025Article
- Systematic characterization of cell type-specific master metabolic regulators in Alzheimer's disease.Research square · 2025Article
- Cell type-specific master metabolic regulators of Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Serum Norepinephrine and Cholesterol Concentrations as Novel Diagnostic Biomarkers for Vitamin E Deficiency in Holstein Cows.Animals : an open access journal from MDPI · 2025Article
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Fatty acids are metabolized by β-oxidation within the "mitochondrial ketogenic pathway" (MKP) to generate β-hydroxybutyrate (BHB), a ketone body. BHB can be generated by most cells but largely by hepatocytes following exercise, fasting, or ketogenic diet consumption. BHB has been shown to modulate systemic and brain inflammation; however, its direct effects on microglia have been little studied. We investigated the impact of BHB on Aβ oligomer (AβO)-stimulated human iPS-derived microglia (hiMG), a model relevant to the pathogenesis of Alzheimer's disease (AD). HiMG responded to AβO with proinflammatory activation, which was mitigated by BHB at physiological concentrations of 0.1-2 mM. AβO stimulated glycolytic transcripts, suppressed genes in the β-oxidation pathway, and induced over-expression of AD-relevant p46Shc, an endogenous inhibitor of thiolase, actions that are expected to suppress MKP. AβO also triggered mitochondrial Ca
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.