Evidence map›Paper›PMID 27907119›Full record

ArticlePloS one2016

Gray Matter Hypoxia in the Brain of the Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis.

Thomas W Johnson, Ying Wu, Nabeela Nathoo, James A Rogers, V Wee Yong, Jeff F Dunn

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Hypoxia in multiple sclerosis.Redox biology · 2025
    Review
  4. Review
  5. Review
  6. The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Oligodendrocyte-Specific Deletion ofInternational journal of molecular sciences · 2021
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Multiple sclerosis disease progression: Contributions from a hypoxia-inflammation cycle.Multiple sclerosis (Houndmills, Basingstoke, England) · 2019
    Article
  19. Article
  20. Article
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 at 1 institution in 1 country.

Thomas W JohnsonDepartment of Radiology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Ying WuDepartment of Radiology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Nabeela NathooDepartment of Radiology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
James A RogersDepartment of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
V Wee YongDepartment of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Jeff F DunnDepartment of Radiology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
University of Calgary · CA

Funding

Development and validation of a multimodal MRI/near-infrared spectroscopysystem to study brain oxidative metabolism in mouse models of neurologicaldiseaseR21EB021397 · NIBIB · UNIVERSITY OF CALGARY · PI DUNN, JEFFREY FRANK · 2016 to 2017
$295k
NIBIB NIH HHS R21 EB021397
6 · The paper itself

Abstract

backgroundMultiple sclerosis (MS) has a significant inflammatory component and may have significant gray matter (GM) pathophysiology. Brain oxygenation is a sensitive measurement of the balance between metabolic need and oxygen delivery. There is evidence that inflammation and hypoxia are interdependent. In this paper, we applied novel, implanted PO2 sensors to measure hypoxia in cortical and cerebellar GM, in an inflammation-induced mouse model of MS.

objectiveQuantify oxygenation in cortical and cerebellar GM in the awake, unrestrained experimental autoimmune encephalomyelitis (EAE) mouse model and to relate the results to symptom level and disease time-course.

methodsC57BL/6 mice were implanted with a fiber-optic sensor in the cerebellum (n = 13) and cortex (n = 24). Animals were induced with stimulation of the immune response and sensitization to myelin oligodendrocyte glycoprotein (MOG). Controls did not have MOG. We measured PO2 in awake, unrestrained animals from pre-induction (baseline) up to 36 days post-induction for EAE and controls.

resultsThere were more days with hypoxia than hyperoxia (cerebellum: 34/67 vs. 18/67 days; cortex: 85/112 vs. 22/112) compared to time-matched controls. The average decline in PO2 on days that were significantly lower than time-matched controls was -8.8±6.0 mmHg (mean ± SD) for the cerebellum and -8.0±4.6 for the cortex. Conversely, the average increase in PO2 on days that were significantly hyperoxic was +3.2±2.8 mmHg (mean ± SD) for the cerebellum and +0.8±2.1 for the cortex. Cortical hypoxia related to increased behavioral deficits. Evidence for hypoxia occurred before measurable behavioral deficits.

conclusionsA highly inflammatory condition primed to a white matter (WM) autoimmune response correlates with significant hypoxia and increased variation in oxygenation in GM of both cerebellum and cortex in the mouse EAE model of MS.

Indexed as

AnimalsBehavior, AnimalBrainCerebellumCerebral CortexDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGray MatterHypoxiaMagnetic Resonance ImagingMiceMultiple SclerosisOxygen ConsumptionTime Factors

Identifiers

PMID27907119
PMCPMC5131950
OpenAlexW2558683541

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.