Evidence map›Paper›PMID 24734229›Full record

ReviewBioMed research international2014

Role of methylglyoxal in Alzheimer's disease.

Cristina Angeloni, Laura Zambonin, Silvana Hrelia

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. 3D human stem-cell-derived neuronal spheroids forCurrent research in toxicology · 2024
    Article
  20. Highly specific σProceedings of the National Academy of Sciences of the United States of America · 2023
    Article

20 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Cristina AngeloniDepartment for Life Quality Studies, Alma Mater Studiorum, University of Bologna, Corso d'Augusto 237, 47900 Rimini, Italy.ORCID 0000-0002-6731-6187
Laura ZamboninDepartment of Pharmacy and Biotechnology, Alma Mater Studiorum, University of Bologna, Via Irnerio 48, 40126 Bologna, Italy.
Silvana HreliaDepartment for Life Quality Studies, Alma Mater Studiorum, University of Bologna, Corso d'Augusto 237, 47900 Rimini, Italy.
University of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is the most common and lethal neurodegenerative disorder. The major hallmarks of Alzheimer's disease are extracellular aggregation of amyloid β peptides and, the presence of intracellular neurofibrillary tangles formed by precipitation/aggregation of hyperphosphorylated tau protein. The etiology of Alzheimer's disease is multifactorial and a full understanding of its pathogenesis remains elusive. Some years ago, it has been suggested that glycation may contribute to both extensive protein cross-linking and oxidative stress in Alzheimer's disease. Glycation is an endogenous process that leads to the production of a class of compounds known as advanced glycation end products (AGEs). Interestingly, increased levels of AGEs have been observed in brains of Alzheimer's disease patients. Methylglyoxal, a reactive intermediate of cellular metabolism, is the most potent precursor of AGEs and is strictly correlated with an increase of oxidative stress in Alzheimer's disease. Many studies are showing that methylglyoxal and methylglyoxal-derived AGEs play a key role in the etiopathogenesis of Alzheimer's disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAntioxidantsGlycation End Products, AdvancedGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansOxidation-ReductionOxidative Stressp38 Mitogen-Activated Protein KinasesPC12 CellsPhosphorylationPyruvaldehydeRatsRisk FactorsAmyloid beta-PeptidesAntioxidantsGlycation End Products, AdvancedGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betap38 Mitogen-Activated Protein KinasesPyruvaldehydetau Proteins

Identifiers

PMID24734229
PMCPMC3966409
OpenAlexW2027098171

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.