ArticleJournal of clinical biochemistry and nutrition2025
Aging-related dysregulation of energy metabolism and mitochondrial dynamics in microglia.
Article in Journal of clinical biochemistry and nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Exploring Early Neurodegeneration Through Fasting-Induced Metabolic Signatures and High-Sensitivity Biomarkers.Current issues in molecular biology · 2026Review
- Cholinergic regulation of neuroinflammation: linking microglia, immunometabolism, and neuromodulation.Frontiers in immunology · 2026Review
- Esketamine Attenuates Postoperative Neurocognitive Disorder in Aged Mice: Associations with Bioenergetic Remodeling in Hippocampal CD11b-Enriched Cell Fractions and Glycolysis-Related Signaling.Drug design, development and therapy · 2026Article
- Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.Life (Basel, Switzerland) · 2025Review
- Scoping Review: The Role of Tocotrienol-Rich Fraction as a Potent Neuroprotective Agent.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
Microglia, the primary immune cells of the central nervous system, play a pivotal role in maintaining brain homeostasis. Recent studies have highlighted the involvement of microglial dysfunction in the pathogenesis of various age-related neurodegenerative diseases, such as Alzheimer's disease. Moreover, the metabolic state of microglia has emerged as a key factor in these diseases. Interestingly, aging and neurodegenerative diseases are associated with impaired mitochondrial function and a metabolic shift from oxidative phosphorylation to glycolysis in microglia. This metabolic shift may contribute to sustained microglial activation and neuroinflammation. Furthermore, the leakage of mitochondrial DNA into the cytoplasm, because of mitochondrial dysfunction, has been implicated in triggering inflammatory responses and disrupting brain function. This review summarizes recent advances in understanding the role of microglial metabolic shifts, particularly glycolysis, and mitochondrial dysfunction. It also explores the potential of targeting microglial metabolism, for instance by modulating mitophagy or intervening in specific metabolic pathways, as a novel therapeutic approach for changes in brain function and neurodegenerative diseases associated with aging.
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Registered trials
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 Socratic graph.