Evidence map›Paper›PMID 26690780›Full record

ArticleNeurotoxicity research2016

Methylglyoxal Causes Cell Death in Neural Progenitor Cells and Impairs Adult Hippocampal Neurogenesis.

Hye Jeong Chun, Yujeong Lee, Ah Hyun Kim, Jaewon Lee

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Food science & nutrition · 2024
    Article
  4. Article
  5. Advanced Glycation End-Product Precursor Methylglyoxal May Lead to Development of Alzheimer's Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Article
  6. Mechanisms of cognitive dysfunction in CKD.Nature reviews. Nephrology · 2020
    Review
  7. Protective Evaluation of Compounds Extracted from Root ofMolecules (Basel, Switzerland) · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. 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

4 authors at 1 institution in 1 country.

Hye Jeong ChunDepartment of Pharmacy, College of Pharmacy, Molecular Inflammation Research Center for Aging Intervention, Pusan National University, Busan, 609-735, Republic of Korea.
Yujeong LeeDepartment of Pharmacy, College of Pharmacy, Molecular Inflammation Research Center for Aging Intervention, Pusan National University, Busan, 609-735, Republic of Korea.
Ah Hyun KimDepartment of Pharmacy, College of Pharmacy, Molecular Inflammation Research Center for Aging Intervention, Pusan National University, Busan, 609-735, Republic of Korea.
Jaewon LeeDepartment of Pharmacy, College of Pharmacy, Molecular Inflammation Research Center for Aging Intervention, Pusan National University, Busan, 609-735, Republic of Korea. neuron@pusan.ac.kr.
Pusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methylglyoxal (MG) is formed during normal metabolism by processes like glycolysis, lipid peroxidation, and threonine catabolism, and its accumulation is associated with various degenerative diseases, such as diabetes and arterial atherogenesis. Furthermore, MG has also been reported to have toxic effects on hippocampal neurons. However, these effects have not been studied in the context of neurogenesis. Here, we report that MG adversely affects hippocampal neurogenesis and induces neural progenitor cell (NPC) death. MG significantly reduced C17.2 NPC proliferation, and high concentration of MG (500 μM) induced cell death and elevated oxidative stress. Further, MG was found to activate the ERK signaling pathway, indicating elevated stress response. To determine the effects of MG in vivo, mice were administrated with vehicle or MG (0.5 or 1 % in drinking water) for 4 weeks. The numbers of BrdU-positive cells in hippocampi were significantly lower in MG-treated mice, indicating impaired neurogenesis, but MG did not induce neuronal damage or glial activations. Interestingly, MG reduced memory retention when administered to mice at 1 % but not at 0.5 %. In addition, the levels of hippocampal BDNF and synaptophysin were significantly lower in the hippocampi of mice treated with MG at 1 %. Collectively, our findings suggest MG could be harmful to NPCs and to hippocampal neurogenesis.

Indexed as

AnimalsAvoidance LearningBrain-Derived Neurotrophic FactorCell DeathCell ProliferationCells, CulturedHippocampusMaleMAP Kinase Signaling SystemMemoryMiceMice, Inbred C57BLNeural Stem CellsNeurogenesisPyruvaldehydeReactive Oxygen SpeciesBrain-Derived Neurotrophic FactorPyruvaldehydeReactive Oxygen SpeciesSynaptophysinBrain-derived neurotropic factorHippocampal neurogenesisMemory retentionMethylglyoxalNeural progenitor cells

Identifiers

PMID26690780
OpenAlexW2207093236

What OpenQuestion holds

Textmetadata
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.