Deoxyglucose prevents neurodegeneration in culture by eliminating microglia
Open accessAbstract
BACKGROUND: 2-Deoxy-D-glucose is an inhibitor of glycolysis, which is protective in animal models of brain pathology, but the mechanisms of this protection are unclear. We examined whether, when and how deoxyglucose protects neurons in co-culture with astrocytes and microglia. Microglia are brain macrophages, which can damage neurons in inflammatory conditions. METHODS: Deoxyglucose was added to primary cultures of microglia and astrocytes from rat cortex, or neurons and glia from rat cerebellum, or the BV-2 microglial cell line, and cell death and cell functions were evaluated. RESULTS: Surprisingly, addition of deoxyglucose induced microglial loss and prevented spontaneous neuronal loss in long-term cultures of neurons and glia, while elimination of microglia by L-leucine-methyl ester prevented the deoxyglucose-induced neuroprotection. Deoxyglucose also prevented neuronal loss induced by addition of amyloid beta or disrupted neurons (culture models of Alzheimer's disease and brain trauma respectively). However, deoxyglucose greatly increased the neuronal death induced by hypoxia. Addition of deoxyglucose to pure microglia induced necrosis and loss, preceded by rapid ATP depletion and followed by phagocytosis of the microglia. Deoxyglucose did not kill astrocytes or neurons. CONCLUSIONS: We conclude that deoxyglucose causes microglial loss by ATP depletion, and this can protect neurons from neurodegeneration, except in conditions of hypoxia. Deoxyglucose may thus be beneficial in brain pathologies mediated by microglia, including brain trauma, but not where hypoxia is involved.
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Inhibition of hexokinase activity by 2-deoxy-D-glucose (2-DG) inhibited the inflammatory response measured as NOS-2 expression in BV2 at 6h without inducing cell death.
“inhibition of hexokinase activity by using 2deoxy-D-glucose (2-DG) inhibited the inflammatory response measured as NOS-2 expression in BV2 at 6h without inducing cell death (Vilalta and Brown, 2014), (Tannahill et al., 2013) (Figure S5F-G).”
From TET2 Regulates the Neuroinflammatory Response in Microglia (2019) · cites this paper as Vilalta and Brown, 2014
The Methods (Flow cytometry; page unavailable) confirm that BV-2 viability was assessed after 6 hours of deoxyglucose treatment. The Results (Microglia are killed by deoxyglucose via ATP depletion and phagocytosis; page unavailable) report ATP depletion before cell death, but do not report reduced NOS-2 expression or establish the claimed absence of cell death at 6 hours. They instead report a small increase in TNFα release from primary microglia at 3 hours. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMicroglia have a metabolic dependence on glycolysis.
“because microglia have a metabolic dependence on glycolysis (Vilalta and Brown, 2014)”
From TET2 Regulates the Neuroinflammatory Response in Microglia (2019) · cites this paper as Vilalta and Brown, 2014
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Additional file 1 of Early glycolytic reprogramming controls microglial inflammatory activation
Cheng, J., Zhang, R., Xu, Z., Ke, Y., Sun, R., Yang, H., Zhang, X., Zhen, X., & Zheng, L.-T. (2021) · Figshare · doi:10.6084/m9.figshare.14759534
In vitro and in vivo study of the effects of Levetiracetam on activated microglia during sepsis
Fleurance, R. (2021) · theses.fr (ABES) · doi:10.70675/0a82ed6ez6595z4366z832fz70cbe839c7ff
- Authors
- Vilalta, A., & Brown, G. C.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Brown, Guy C
- Venue
- Journal of Neuroinflammation
- Published
- 2014
- Volume
- 11
- Issue
- 1
- Pages
- 58
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3986974
- OpenAlex
- W2125189608
- Cited by
- 58
- References
- 37
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 8 · 2023: 5 · 2022: 8 · 2021: 8 · 2020: 3 · 2019: 5 · 2018: 3 · 2017: 5 · 2016: 1 · 2015: 4
- FWCI
- 1.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- European Commission (251867)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- 2-deoxyglucose, microglia, neuroprotection, neurodegeneration, glycolysis inhibition, ATP depletion, neuronal cell death, amyloid-beta, traumatic brain injury, hypoxia, L-leucine methyl ester, phagocytosis, astrocytes, Alzheimer's disease, BV-2 cells
- MeSH terms
- Animals, Animals, Newborn, Hypoxia, Cell Count, Cells, Cultured, Cerebellum, Deoxyglucose, Female, Male, Neurons, Phagocytosis, Time Factors, Tumor Necrosis Factor-alpha, Wounds and Injuries, Amyloid beta-Peptides, Cell Death, Rats, Wistar, Microglia, Neuroprotective Agents
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