Evidence map›Paper›PMID 39251890›Full record

ArticleNature neuroscience2024

Oligodendroglial fatty acid metabolism as a central nervous system energy reserve.

Ebrahim Asadollahi, Andrea Trevisiol, Aiman S Saab, Zoe J Looser, Payam Dibaj, Reyhane Ebrahimi, Kathrin Kusch, Torben Ruhwedel, Wiebke Möbius, Olaf Jahn and 13 more

Erratum issuedAbstract read
In one paragraph

Article in Nature neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
–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

82 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. ENT1 inhibition links oligodendrocyte lipid metabolism to connectivity in tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors.

Ebrahim AsadollahiMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany. asadollahi@mpinat.mpg.de.ORCID http://orcid.org/0000-0003-4737-3587
Andrea TrevisiolMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany.
Aiman S SaabMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany.ORCID http://orcid.org/0000-0003-3886-8369
Zoe J LooserUniversity of Zurich, Institute of Pharmacology and Toxicology, Zurich, Switzerland.
Payam DibajMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany.
Reyhane EbrahimiMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany.
Kathrin KuschMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany.ORCID http://orcid.org/0000-0002-5079-502X
Torben RuhwedelMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany.ORCID http://orcid.org/0000-0002-9535-9395
Wiebke MöbiusMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany.ORCID http://orcid.org/0000-0002-2902-7165
Olaf JahnMax Planck Institute for Multidisciplinary Sciences, Department of Molecular Neurobiology, Neuroproteomics Group, Göttingen, Germany.ORCID http://orcid.org/0000-0002-3397-8924
Jun Yup LeeSchool of Medical Sciences and Charles Perkins Centre, The University of Sydney, Camperdown, New South Wales, Australia.
Anthony S DonSchool of Medical Sciences and Charles Perkins Centre, The University of Sydney, Camperdown, New South Wales, Australia.ORCID http://orcid.org/0000-0003-1655-1184
Michelle-Amirah KhalilDepartment for Bioinformatics and Biochemistry, Braunschweig Integrated Center of System Biology, Technische Universität Braunschweig, Braunschweig, Germany.
Karsten HillerDepartment for Bioinformatics and Biochemistry, Braunschweig Integrated Center of System Biology, Technische Universität Braunschweig, Braunschweig, Germany.
Myriam BaesLab of Cell Metabolism, Department of Pharmaceutical and Pharmacological Sciences, KU Leuven, Leuven, Belgium.
Bruno WeberUniversity of Zurich, Institute of Pharmacology and Toxicology, Zurich, Switzerland.ORCID http://orcid.org/0000-0002-9089-0689
E Dale AbelDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Andrea BallabioTelethon Institute of Genetics and Medicine, Naples, Italy.ORCID http://orcid.org/0000-0003-1381-4604
Brian PopkoFeinberg School of Medicine, Northwestern University, Chicago, IL, USA.ORCID http://orcid.org/0000-0001-9948-2553
Celia M KassmannMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany.
Hannelore EhrenreichMax Planck Institute for Multidisciplinary Sciences, Clinical Neuroscience, Göttingen, Germany.ORCID http://orcid.org/0000-0001-8371-5711
Johannes HirrlingerMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany.ORCID http://orcid.org/0000-0002-6327-0089
Klaus-Armin NaveMax Planck Institute for Multidisciplinary Sciences, Department of Neurogenetics, Göttingen, Germany. nave@mpinat.mpg.de.ORCID http://orcid.org/0000-0001-8724-9666

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) SPP1757Deutsche Forschungsgemeinschaft (German Research Foundation) TRR-274
6 · The paper itself

Abstract

Brain function requires a constant supply of glucose. However, the brain has no known energy stores, except for glycogen granules in astrocytes. In the present study, we report that continuous oligodendroglial lipid metabolism provides an energy reserve in white matter tracts. In the isolated optic nerve from young adult mice of both sexes, oligodendrocytes survive glucose deprivation better than astrocytes. Under low glucose, both axonal ATP levels and action potentials become dependent on fatty acid β-oxidation. Importantly, ongoing oligodendroglial lipid degradation feeds rapidly into white matter energy metabolism. Although not supporting high-frequency spiking, fatty acid β-oxidation in mitochondria and oligodendroglial peroxisomes protects axons from conduction blocks when glucose is limiting. Disruption of the glucose transporter GLUT1 expression in oligodendrocytes of adult mice perturbs myelin homeostasis in vivo and causes gradual demyelination without behavioral signs. This further suggests that the imbalance of myelin synthesis and degradation can underlie myelin thinning in aging and disease.

Indexed as

Energy MetabolismFatty AcidsOligodendrogliaAction PotentialsAdenosine TriphosphateAnimalsAstrocytesCentral Nervous SystemFemaleGlucoseGlucose Transporter Type 1Lipid MetabolismMaleMiceMice, Inbred C57BLMice, TransgenicAdenosine TriphosphateFatty AcidsGlucoseGlucose Transporter Type 1Slc2a1 protein, mouse

Identifiers

PMID39251890
PMCPMC11452346

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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.