ArticleRedox biology2021
Combined glyoxalase 1 dysfunction and vitamin B6 deficiency in a schizophrenia model system causes mitochondrial dysfunction in the prefrontal cortex.
Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Examining glycation as a mediator linking bullying to psychotic experience and depressive symptom in adolescents.Molecular psychiatry · 2026Article
- Ryanodine receptor 2-mediated calcium leak is associated with increased glyoxalase I in the aging brain.JCI insight · 2025Article
- Characterization of SPTLC2 as a key driver promoting microglial activation and energy metabolism reprogramming after ischemic stroke through bulk and single-cell analyses combined with experimental validation.Cell biology and toxicology · 2025Article
- Mitochondrial dysfunction by glyoxalase 1 deficiency disrupts definitive endoderm and alveolar development of human pluripotent stem cells.Experimental & molecular medicine · 2025Article
- Substantia nigra related gene polymorphisms associated with antipsychotic-induced acute movement disorders: a genome-wide association study and multi-ancestry validation in schizophrenia.Military Medical Research · 2025Article
- Exploring the molecular mechanism of Tripterygium Wilfordii Hook F in treating systemic lupus erythematosus via network pharmacology and molecular docking.Clinical rheumatology · 2025Article
- Dimethyl Fumarate Reduces Methylglyoxal-derived Carbonyl Stress Through Nrf2/GSH Activation in SH-SY5Y Cells.Neurochemical research · 2024Article
- Mitochondrial dysfunction in psychiatric disorders.Schizophrenia research · 2024Review
- Potential Immunohistochemical Biomarkers for Grading Oral Dysplasia: A Literature Review.Biomedicines · 2024Review
- Association between enhanced carbonyl stress and decreased apparent axonal density in schizophrenia by multimodal white matter imaging.Scientific reports · 2023Article
- Identification of PIK3CG as a hub in septic myocardial injury using network pharmacology and weighted gene co-expression network analysis.Bioengineering & translational medicine · 2023Article
- Changes in S-(2-succinyl)cysteine and advanced glycation end-products levels in mouse tissues associated with aging.Amino acids · 2022Article
- High-sucrose diets contribute to brain angiopathy with impaired glucose uptake and psychosis-related higher brain dysfunctions in mice.Science advances · 2021Article
- Glyoxalase 1 Confers Susceptibility to Schizophrenia: From Genetic Variants to Phenotypes of Neural Function.Frontiers in molecular neuroscience · 2021Article
- Genetic polymorphism and neuroanatomical changes in schizophrenia.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
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Authors and funding
20 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylglyoxal (MG) is a reactive and cytotoxic α-dicarbonyl byproduct of glycolysis. Our bodies have several bio-defense systems to detoxify MG, including an enzymatic system by glyoxalase (GLO) 1 and GLO2. We identified a subtype of schizophrenia patients with novel mutations in the GLO1 gene that results in reductions of enzymatic activity. Moreover, we found that vitamin B6 (VB6) levels in peripheral blood of the schizophrenia patients with GLO1 dysfunction are significantly lower than that of healthy controls. However, the effects of GLO1 dysfunction and VB6 deficiency on the pathophysiology of schizophrenia remains poorly understood. Here, we generated a novel mouse model for this subgroup of schizophrenia patients by feeding Glo1 knockout mice VB6-deficent diets (KO/VB6(-)) and evaluated the combined effects of GLO1 dysfunction and VB6 deficiency on brain function. KO/VB6(-) mice accumulated homocysteine in plasma and MG in the prefrontal cortex (PFC), hippocampus, and striatum, and displayed behavioral deficits, such as impairments of social interaction and cognitive memory and a sensorimotor deficit in the prepulse inhibition test. Furthermore, we found aberrant gene expression related to mitochondria function in the PFC of the KO/VB6(-) mice by RNA-sequencing and weighted gene co-expression network analysis (WGCNA). Finally, we demonstrated abnormal mitochondrial respiratory function and subsequently enhanced oxidative stress in the PFC of KO/VB6(-) mice in the PFC. These findings suggest that the combination of GLO1 dysfunction and VB6 deficiency may cause the observed behavioral deficits via mitochondrial dysfunction and oxidative stress in the PFC.
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