ReviewImmunological reviews2025
Ketone body metabolism and the NLRP3 inflammasome in Alzheimer's disease.
Review in Immunological reviews, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed.
- The roles of microglia and astrocytes in inflammasomes and neurological disorders.Neural regeneration research · 2026Article
- Selective inhibition of monoamine oxidase B represents a therapeutic strategy for diabetic peripheral neuropathy.Acta pharmacologica Sinica · 2026Article
- Decoding neuroinflammation: the critical role of NLRP3 inflammasome in Alzheimer's disease.Inflammopharmacology · 2026Review
- A perspective for alzheimer disease from gut microbiota-associated NMR-based fecal metabolomics: a study with 5XFAD mice.Metabolic brain disease · 2026Article
- β-Hydroxybutyrate attenuates glycation-induced structural destabilization and amyloidogenic aggregation in human serum albumin.Biochemistry and biophysics reports · 2026Article
- HMGCS2-dependent β-OHB/H3K9bhb ameliorates synaptic plasticity and cognition in Alzheimer's disease.Experimental & molecular medicine · 2026Article
- Mitochondrial dysfunction in Alzheimer's disease: targeting the powerhouse with nanomedicine.Frontiers in pharmacology · 2026Review
- Mechanisms of energy metabolism reprogramming and homeostasis maintenance in overwintering hibernating animals.Frontiers in veterinary science · 2026Review
- Nutritional substrates and microglial metabolic fitness in brain aging and Alzheimer's disease: from lipid handling to TREM2-linked translation.Frontiers in nutrition · 2026Review
- Demystifying anti-inflammatory therapeutic strategies against pancreatitis and concomitant diseases: a 2025 perspective.Theranostics · 2026Review
- Ketogenic metabolic therapy: low-carbohydrate interventions as novel neuroprotective strategies for cognitive dysfunction in diabetes.Frontiers in aging neuroscience · 2026Review
- [Mediation analysis of plasma phosphorylated tau217 in the association between periodontitis and mild cognitive impairment].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2025Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- Exercise orchestrates systemic metabolic and neuroimmune homeostasis via the brain-muscle-liver axis to slow down aging and neurodegeneration: a narrative review.European journal of medical research · 2025Review
- Chaperone-mediated autophagy, heat shock protein 70, and serotonin: novel targets of beta-hydroxybutyrate in HFFD/LPS-induced sporadic Alzheimer's disease model.Inflammopharmacology · 2025Article
- Innate Immune Sensors in Health and Disease.Immunological reviews · 2025Article
- New insights into the molecular biology of Alzheimer's-like cerebral amyloidosis achieved through multi-omics approaches.PloS one · 2025Article
- Ketone body metabolism and the NLRP3 inflammasome in Alzheimer's disease.Immunological reviews · 2025Review
- Exogenous Ketones in Cardiovascular Disease and Diabetes: From Bench to Bedside.Journal of clinical medicine · 2024Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Alzheimer's disease (AD) is a degenerative brain disorder and the most common form of dementia. AD pathology is characterized by senile plaques and neurofibrillary tangles (NFTs) composed of amyloid-β (Aβ) and hyperphosphorylated tau, respectively. Neuroinflammation has been shown to drive Aβ and tau pathology, with evidence suggesting the nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome as a key pathway in AD pathogenesis. NLRP3 inflammasome activation in microglia, the primary immune effector cells of the brain, results in caspase-1 activation and secretion of IL-1β and IL-18. Recent studies have demonstrated a dramatic interplay between the metabolic state and effector functions of immune cells. Microglial metabolism in AD is of particular interest, as ketone bodies (acetone, acetoacetate (AcAc), and β-hydroxybutyrate (BHB)) serve as an alternative energy source when glucose utilization is compromised in the brain of patients with AD. Furthermore, reduced cerebral glucose metabolism concomitant with increased BHB levels has been demonstrated to inhibit NLRP3 inflammasome activation. Here, we review the role of the NLRP3 inflammasome and microglial ketone body metabolism in AD pathogenesis. We also highlight NLRP3 inflammasome inhibition by several ketone body therapies as a promising new treatment strategy for AD.
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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.