Evidence map›Paper›PMID 31068938›Full record

ArticleFrontiers in immunology2019

Methylglyoxal-Derived Advanced Glycation Endproducts Accumulate in Multiple Sclerosis Lesions.

Suzan Wetzels, Tim Vanmierlo, Jean L J M Scheijen, Jack van Horssen, Sandra Amor, Veerle Somers, Casper G Schalkwijk, Jerome J A Hendriks, Kristiaan Wouters

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Low Serum Methylglyoxal Levels Correlate with Psoriasis Severity and Inflammatory Response Indices.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Metabolic Control of Microglia.Advances in neurobiology · 2024
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
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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

9 authors at 4 institutions in 2 countries.

Suzan WetzelsCardiovascular Research Institute Maastricht, Department of Internal Medicine, Maastricht University, Maastricht, Netherlands.
Tim VanmierloBiomedical Research Institute, Department of Immunology and Biochemistry, Hasselt University, Hasselt, Belgium.
Jean L J M ScheijenCardiovascular Research Institute Maastricht, Department of Internal Medicine, Maastricht University, Maastricht, Netherlands.
Jack van HorssenDepartment of Molecular Cell Biology and Immunology, Amsterdam UMC, Vrije Universiteit, Amsterdam, Netherlands.
Sandra AmorDepartment of Pathology, Amsterdam UMC, VU University Medical Center, Amsterdam, Netherlands.
Veerle SomersBiomedical Research Institute, Department of Immunology and Biochemistry, Hasselt University, Hasselt, Belgium.
Casper G SchalkwijkCardiovascular Research Institute Maastricht, Department of Internal Medicine, Maastricht University, Maastricht, Netherlands.
Jerome J A HendriksBiomedical Research Institute, Department of Immunology and Biochemistry, Hasselt University, Hasselt, Belgium.
Kristiaan WoutersCardiovascular Research Institute Maastricht, Department of Internal Medicine, Maastricht University, Maastricht, Netherlands.
Maastricht University · NLHasselt University · BEAmsterdam UMC Location VUmc · NLAmsterdam University Medical Centers · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a demyelinating autoimmune disease in which innate and adaptive immune cells infiltrate the central nervous system (CNS) and damage the myelin sheaths surrounding the axons. Upon activation, infiltrated macrophages, CNS-resident microglia, and astrocytes switch their metabolism toward glycolysis, resulting in the formation of α-dicarbonyls, such as methylglyoxal (MGO) and glyoxal (GO). These potent glycating agents lead to the formation of advanced glycation endproducts (AGEs) after reaction with amino acids. We hypothesize that AGE levels are increased in MS lesions due to the inflammatory activation of macrophages and astrocytes. First, we measured tissue levels of AGEs in brain samples of MS patients and controls. Analysis of MS patient and non-demented control (NDC) specimens showed a significant increase in protein-bound N

Indexed as

AgedAstrocytesBiomarkersDisease ProgressionDisease SusceptibilityFemaleGlycation End Products, AdvancedHumansImmunohistochemistryMaleMicrogliaMiddle AgedMultiple SclerosisPyruvaldehydeBiomarkersGlycation End Products, AdvancedPyruvaldehydeadvanced glycation endproductsastrocytesmultiple sclerosisneuroinflammationα-dicarbonyl

Identifiers

PMID31068938
PMCPMC6491451
OpenAlexW2942312619

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.