ArticleNeurochemical research2020
Repeated Methylglyoxal Treatment Depletes Dopamine in the Prefrontal Cortex, and Causes Memory Impairment and Depressive-Like Behavior in Mice.
Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Quantifying the inverted U: A meta-analysis of prefrontal dopamine, D1 receptors, and working memory.Behavioral neuroscience · 2022Pooled it
- 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
- Methylglyoxal Affects Dopamine Homeostasis in SH-SY5Y Cells Through the Modulation of miR-190a and miR-214.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Propyl Gallate Attenuates Methylglyoxal-Induced Alzheimer-like Cognitive Deficits and Neuroinflammation in Mice.International journal of molecular sciences · 2026Article
- Deep learning identifies TP-41 for methylglyoxal scavenging in Alzheimer's treatment.Theranostics · 2026Article
- Deciphering the mechanisms by which probioticCurrent research in food science · 2026Article
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
- Gender-Dependent Cognitive and Metabolic Benefits Due to Glyoxalase 1 (Glo1) Overexpression in Age-Accelerated SAMP8 Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025Review
- Glucose Metabolic Abnormality: A Crosstalk between Depression and Alzheimer's Disease.Current neuropharmacology · 2025Review
- Synaptotagmin-4 induces anhedonic responses to chronic stress via BDNF signaling in the medial prefrontal cortex.Experimental & molecular medicine · 2024Article
- Article
- Combination of Walnut Peptide and Casein Peptide alleviates anxiety and improves memory in anxiety mices.Frontiers in nutrition · 2023Article
- Arginine Reduces Glycation in γCells · 2022Article
- Sex-Dependent Alterations in the mRNA Expression of Enzymes Involved in Dopamine Synthesis and Breakdown After Methamphetamine Self-Administration.Neurotoxicity research · 2022Article
- Sex-Specific Alterations in Dopamine Metabolism in the Brain after Methamphetamine Self-Administration.International journal of molecular sciences · 2022Article
- Fentanyl-induced acute and conditioned behaviors in two inbred mouse lines: Potential role for Glyoxalase.Physiology & behavior · 2022Article
- Advanced Glycation End-Product Precursor Methylglyoxal May Lead to Development of Alzheimer's Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Diabetes and Cognitive Impairment: A Role for Glucotoxicity and Dopaminergic Dysfunction.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Methylglyoxal (MGO) is a highly reactive dicarbonyl molecule that promotes the formation of advanced glycation end products (AGEs), which are believed to play a key role in a number of pathologies, such as diabetes, Alzheimer's disease, and inflammation. Here, Swiss mice were treated with MGO by intraperitoneal injection to investigate its effects on motor activity, mood, and cognition. Acute MGO treatment heavily decreased locomotor activity in the open field test at higher doses (80-200 mg/kg), an effect not observed at lower doses (10-50 mg/kg). Several alterations were observed 4 h after a single MGO injection (10-50 mg/kg): (a) plasma MGO levels were increased, (b) memory was impaired (object location task), (c) anxiolytic behavior was observed in the open field and marble burying test, and (d) depressive-like behavior was evidenced as evaluated by the tail suspension test. Biochemical alterations in the glutathione and glyoxalase systems were not observed 4 h after MGO treatment. Mice were also treated daily with MGO at 0, 10, 25 and 50 mg/kg for 11 days. From the 5th to the 11th day, several behavioral end points were evaluated, resulting in: (a) absence of motor impairment as evaluated in the open field, horizontal bars and pole test, (b) depressive-like behavior observed in the tail suspension test, and (c) cognitive impairments detected on working, short- and long-term memory when mice were tested in the Y-maze spontaneous alternation, object location and recognition tests, and step-down inhibitory avoidance task. An interesting finding was a marked decrease in dopamine levels in the prefrontal cortex of mice treated with 50 mg/kg MGO for 11 days, along with a ~ 25% decrease in the Glo1 content. The MGO-induced dopamine depletion in the prefrontal cortex may be related to the observed memory deficits and depressive-like behavior, an interesting topic to be further studied as a potentially novel route for MGO toxicity.
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Registered trials
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