Evidence map›Paper›PMID 37408029›Full record

ArticleActa neuropathologica communications2023

Mechanisms of metabolic stress induced cell death of human oligodendrocytes: relevance for progressive multiple sclerosis.

Milton Guilherme Forestieri Fernandes, Abdulshakour Mohammadnia, Florian Pernin, Laura Eleonora Schmitz-Gielsdorf, Caroline Hodgins, Qiao-Ling Cui, Moein Yaqubi, Manon Blain, Jeffery Hall, Roy Dudley and 10 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.1field-weighted citation impact, top 5% of its field
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

11 citing papers in PubMed, 19 citations in OpenAlex.

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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

20 authors at 6 institutions in 3 countries.

Milton Guilherme Forestieri FernandesNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Abdulshakour MohammadniaNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Florian PerninNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Laura Eleonora Schmitz-GielsdorfInstitute of Neuropathology, University Hospital Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Germany.
Caroline HodginsNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Qiao-Ling CuiNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Moein YaqubiNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Manon BlainNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Jeffery HallDepartment of Neurosurgery, Department of Neurology and Neurosurgery, McGill University Health Centre, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Roy DudleyDepartment of Pediatric Neurosurgery, Montreal Children's Hospital, 1001 Decarie Blvd, Montreal, QC, H4A 3J1, Canada.
Myriam SrourDivision of Pediatric Neurology, Montreal Children's Hospital, 1001 Decarie Blvd, Montreal, QC, H4A 3J1, Canada.
Stephanie E J ZandeeDepartment of Neuroscience, Faculty of Medicine, Université de Montréal, Pavillon Roger- Gaudry, 2900 Edouard Montpetit Blvd, Montreal, QC, H3T 1J4, Canada.
Wendy KlementDepartment of Neuroscience, Faculty of Medicine, Université de Montréal, Pavillon Roger- Gaudry, 2900 Edouard Montpetit Blvd, Montreal, QC, H3T 1J4, Canada.
Alexandre PratDepartment of Neuroscience, Faculty of Medicine, Université de Montréal, Pavillon Roger- Gaudry, 2900 Edouard Montpetit Blvd, Montreal, QC, H3T 1J4, Canada.
Jo Anne StrattonNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Moses RodriguezDepartment of Neurology, Mayo Clinic Foundation, 1216 2nd St SW, Rochester, MN, 55902, USA.
Tanja KuhlmannInstitute of Neuropathology, University Hospital Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Germany.
Wayne MooreNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Timothy E KennedyNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada.
Jack P AntelNeuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. jack.antel@mcgill.ca.ORCID 0000-0002-5148-0636
Montreal Neurological Institute and Hospital · CAUniversité de Montréal · CAMontreal Children's Hospital · CAUniversity Hospital Münster · DEMayo Clinic · USMcGill University Health Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oligodendrocyte (OL) injury and loss are central features of evolving lesions in multiple sclerosis. Potential causative mechanisms of OL loss include metabolic stress within the lesion microenvironment. Here we use the injury response of primary human OLs (hOLs) to metabolic stress (reduced glucose/nutrients) in vitro to help define the basis for the in situ features of OLs in cases of MS. Under metabolic stress in vitro, we detected reduction in ATP levels per cell that precede changes in survival. Autophagy was initially activated, although ATP levels were not altered by inhibitors (chloroquine) or activators (Torin-1). Prolonged stress resulted in autophagy failure, documented by non-fusion of autophagosomes and lysosomes. Consistent with our in vitro results, we detected higher expression of LC3, a marker of autophagosomes in OLs, in MS lesions compared to controls. Both in vitro and in situ, we observe a reduction in nuclear size of remaining OLs. Prolonged stress resulted in increased ROS and cleavage of spectrin, a target of Ca

Indexed as

Multiple SclerosisMultiple Sclerosis, Chronic ProgressiveAdenosine TriphosphateCell DeathHumansOligodendrogliaReactive Oxygen SpeciesAdenosine TriphosphateReactive Oxygen SpeciesCell survivalDemyelinationMyelinNeurodegenerationNeurodegenerative disease

Identifiers

PMID37408029
PMCPMC10320974
OpenAlexW4383264094

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.