ArticleBiological research2024
Depression like-behavior and memory loss induced by methylglyoxal is associated with tryptophan depletion and oxidative stress: a new in vivo model of neurodegeneration.
Article in Biological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Visualized knowledge mapping on the current research trends and emerging areas of neuroimmune modulation in the past two decades.Frontiers in immunology · 2025Pooled it
- Strain-resolved metabolomic chemotyping identifies tryptophan and γ-glutamyl peptides as MGO-AGEs breaking postbiotic compounds for carbonyl stress mitigation.Gut microbes · 2026Article
- Article
- Methylglyoxal mildly impairs spatial memory and reduces expression of excitatory synaptic genes in the hippocampus of male mice.Physiological reports · 2026Article
- Methylglyoxal Accumulation is Associated with Brain Inflammation after Myocardial Infarction with Sex and Regional Differences.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting Glyoxalase-1 Pathway with Natural Compounds: A Translational Strategy to Reduce Dicarbonyl Stress and Prevent Chronic Diseases.Life (Basel, Switzerland) · 2026Review
- Electroacupuncture promotes BDNF-dependent neurogenesis via microglial reprogramming in a chronic stress model.Chinese medicine · 2026Article
- Bacteria from foods and gut microbiota produce methylglyoxal and this metabolite leads to the formation of bioactive 1-acetyl-β-carboline alkaloids.Scientific reports · 2026Article
- Fucoxanthin attenuates carbonyl stress and neuroinflammation by modulating MGO/RAGE/NF-κB axis in Aβ-induced models.Frontiers in pharmacology · 2026Article
- Deep learning identifies TP-41 for methylglyoxal scavenging in Alzheimer's treatment.Theranostics · 2026Article
- Glioblastoma pathophysiology: roles of aging driven changes in STAT3 interactions with NF-κB dimer components in the modulation of the mitochondrial melatonergic pathway and night-time inflammation resolution.Exploration of targeted anti-tumor therapy · 2026Review
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
- Mitigation ofJournal of microbiology and biotechnology · 2025Article
- Biotransformation by beta glucosidase enhances anti inflammatory metabolites in licorice using untargeted metabolomics.NPJ science of food · 2025Article
- 2',4',6'-Trimethoxyacetophenone Isolated fromBiomolecules & therapeutics · 2025Article
- Nicotinamide Adenine Dinucleotide Supplementation Improves Cuprizone-Induced Multiple Sclerosis-Related Behavioral Changes in C57BL/6J Mice.Brain and behavior · 2025Article
- Article
- Review
- Article
- The Comparison Between Dietary Vitamin A Deficiency and the CRP Level in Alzheimer's Disease in Patients with Type 2 Diabetes: A Case-Control Study.Current Alzheimer research · 2025Article
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10 authors.
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Abstract
backgroundDepression and memory loss are prevalent neurodegenerative disorders, with diabetic patients facing an elevated risk of brain dysfunction. Methylglyoxal (MGO) formation, which is heightened in diabetes owing to hyperglycemia and gut dysbiosis, may serve as a critical link between diabetes and brain diseases. Despite the high prevalence of MGO, the precise mechanisms underlying MGO-induced depression and memory loss remain unclear.
resultsWe investigated the effect of MGO stress on depression like-behavior and memory loss to elucidate the potential interplay between MGO-induced tryptophan (Trp) metabolism impairment and oxidative stress in the brain. It demonstrates that MGO induces depression-like behavior in mice, as confirmed by the OFT, TST, FST, SPT, and EPM behavioral tests. MGO led to the depletion of Trp and related neurotransmitters as 5-HT, EPI, and DA in the mouse brain. Additionally, MGO reduced the cell count in the DG, CA1, and CA3 hippocampal regions and modulated TPH2 levels in the brain. Notably, co-treatment with MGO and Trp mirrored the effects observed after Trp-null treatment in neurons, including reduced TPH1 and TPH2 levels and inhibition of neuronal outgrowth. Furthermore, MGO significantly altered the expression of key proteins associated with neurodegeneration, such as p-Tau, p-GSK-3β, APP, oAβ, BDNF, NGF, and p-TrkB. Concurrently, MGO activated MAPKs through ROS induction, triggering a redox imbalance by downregulating Nrf-2, Ho-1, TXNRD1, Trx, Sirt-3, and Sirt-5 expression levels, NAD
conclusionsOur data revealed that MGO-induced depression like-behavior and memory deficits resulted from disturbances in Trp, 5-HT, BDNF, and NGF levels, increased p-Tau and APP expression, neuroinflammation, and impaired redox status (Nrf-2/Ho-1/TXNRD1/Sirt3/5) in the brain.
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