Evidence map›Paper›PMID 38909138›Full record

ArticleScientific reports2024

Metabolic flexibility ensures proper neuronal network function in moderate neuroinflammation.

Bruno Chausse, Nikolai Malorny, Andrea Lewen, Gernot Poschet, Nikolaus Berndt, Oliver Kann

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Antioxidant and Anti-Inflammatory Effects of InhaledPlants (Basel, Switzerland) · 2026
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  12. Extracellular RNAs as Messengers and Early Biomarkers in Neurodegeneration.International journal of molecular sciences · 2025
    Review
  13. Review
  14. Article
  15. Microglia-to-neuron signaling linksProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Bruno ChausseInstitute of Physiology and Pathophysiology, Heidelberg University, Im Neuenheimer Feld 326, 69120, Heidelberg, Germany. bruno.chaussedefreitas@med.uni-heidelberg.de.ORCID http://orcid.org/0000-0001-8397-6890
Nikolai MalornyInstitute of Physiology and Pathophysiology, Heidelberg University, Im Neuenheimer Feld 326, 69120, Heidelberg, Germany.
Andrea LewenInstitute of Physiology and Pathophysiology, Heidelberg University, Im Neuenheimer Feld 326, 69120, Heidelberg, Germany.
Gernot PoschetMetabolomics Core Technology Platform, Centre for Organismal Studies, Heidelberg University, 69120, Heidelberg, Germany.
Nikolaus BerndtDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558, Nuthetal, Germany.
Oliver KannInstitute of Physiology and Pathophysiology, Heidelberg University, Im Neuenheimer Feld 326, 69120, Heidelberg, Germany. oliver.kann@physiologie.uni-heidelberg.de.ORCID http://orcid.org/0000-0003-4365-8067

Funding

Deutsche Forschungsgemeinschaft ZUK 40/2010-3009262
6 · The paper itself

Abstract

Microglia, brain-resident macrophages, can acquire distinct functional phenotypes, which are supported by differential reprogramming of cell metabolism. These adaptations include remodeling in glycolytic and mitochondrial metabolic fluxes, potentially altering energy substrate availability at the tissue level. This phenomenon may be highly relevant in the brain, where metabolism must be precisely regulated to maintain appropriate neuronal excitability and synaptic transmission. Direct evidence that microglia can impact on neuronal energy metabolism has been widely lacking, however. Combining molecular profiling, electrophysiology, oxygen microsensor recordings and mathematical modeling, we investigated microglia-mediated disturbances in brain energetics during neuroinflammation. Our results suggest that proinflammatory microglia showing enhanced nitric oxide release and decreased CX3CR1 expression transiently increase the tissue lactate/glucose ratio that depends on transcriptional reprogramming in microglia, not in neurons. In this condition, neuronal network activity such as gamma oscillations (30-70 Hz) can be fueled by increased ATP production in mitochondria, which is reflected by elevated oxygen consumption. During dysregulated inflammation, high energy demand and low glucose availability can be boundary conditions for neuronal metabolic fitness as revealed by kinetic modeling of single neuron energetics. Collectively, these findings indicate that metabolic flexibility protects neuronal network function against alterations in local substrate availability during moderate neuroinflammation.

Indexed as

Energy MetabolismGlucoseMicrogliaNeuroinflammatory DiseasesNeuronsAdenosine TriphosphateAnimalsBrainInflammationLactic AcidMaleMiceMice, Inbred C57BLMitochondriaNerve NetNitric OxideAdenosine TriphosphateGlucoseLactic AcidNitric OxideGlycolysisImmunometabolismLactate oxidationMicrogliaNeuronal oscillations

Identifiers

PMID38909138
PMCPMC11193723

What OpenQuestion holds

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Registered trials

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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.