Evidence map›Paper›PMID 27014271›Full record

ArticleFrontiers in immunology2016

Ongoing Oxidative Stress Causes Subclinical Neuronal Dysfunction in the Recovery Phase of EAE.

Helena Radbruch, Daniel Bremer, Robert Guenther, Zoltan Cseresnyes, Randall Lindquist, Anja E Hauser, Raluca Niesner

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. A Lupin (International journal of molecular sciences · 2024
    Article
  5. Review
  6. Therapeutic Candidates for Alzheimer's Disease: Saponins.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Gypenosides Prevent HJournal of molecular neuroscience : MN · 2020
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  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

7 authors at 2 institutions in 1 country.

Helena RadbruchDepartment of Neuropathology, Charité - Universitätsmedizin Berlin , Berlin , Germany.
Daniel BremerGerman Rheumatism Research Center (DRFZ) a Leibniz Institute , Berlin , Germany.
Robert GuentherGerman Rheumatism Research Center (DRFZ) a Leibniz Institute , Berlin , Germany.
Zoltan CseresnyesGerman Rheumatism Research Center (DRFZ) a Leibniz Institute , Berlin , Germany.
Randall LindquistGerman Rheumatism Research Center (DRFZ) a Leibniz Institute , Berlin , Germany.
Anja E HauserGerman Rheumatism Research Center (DRFZ) a Leibniz Institute, Berlin, Germany; Immundynamics, Charité - Universiätsmedizin Berlin, Berlin, Germany.
Raluca NiesnerGerman Rheumatism Research Center (DRFZ) a Leibniz Institute , Berlin , Germany.
German Rheumatism Research Centre · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most multiple sclerosis (MS) patients develop over time a secondary progressive disease course, characterized histologically by axonal loss and atrophy. In early phases of the disease, focal inflammatory demyelination leads to functional impairment, but the mechanism of chronic progression in MS is still under debate. Reactive oxygen species generated by invading and resident central nervous system (CNS) macrophages have been implicated in mediating demyelination and axonal damage, but demyelination and neurodegeneration proceed even in the absence of obvious immune cell infiltration, during clinical recovery in chronic MS. Here, we employ intravital NAD(P)H fluorescence lifetime imaging to detect functional NADPH oxidases (NOX1-4, DUOX1, 2) and, thus, to identify the cellular source of oxidative stress in the CNS of mice affected by experimental autoimmune encephalomyelitis (EAE) in the remission phase of the disease. This directly affects neuronal function in vivo, as monitored by cellular calcium levels using intravital FRET-FLIM, providing a possible mechanism of disease progression in MS.

Indexed as

calciumEAE/MSFLIM–FRETintravital imagingNOX

Identifiers

PMID27014271
PMCPMC4789534
OpenAlexW2304586246

What Socratic 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 Socratic graph.