The dysbindin gene (DTNBP1) is located in chromosome 6p22.3, one of the regions of positive linkage for schizophrenia. A strong genetic association between DTNBP1 and schizophrenia has been replicated through many recent studies. In particular, dysbindin protein has been found to play a role in the glutamate neural transmission in the brain. In this study, we attempted to replicate the previously reported positive association between DTNBP1 and schizophrenia in the Korean population. Our sample included 194 patients with schizophrenia based on DSM-IV and 351 normal controls. We genotyped five SNPs including SNP A in promoter region of DTNBP1. The allele and genotype association were analyzed and the simulated haplotype was investigated as well. As the result, we could not find a significant association of DTNBP1 with schizophrenia in this Korean sample. Additional analysis of the subgroup of schizophrenia having familial loading of major psychiatric disorders did not show association, either. In summary, DTNBP1 is not likely to be a major susceptibility gene for schizophrenia in this Korean population. This result of no association also implies possible genetic heterogeneity of schizophrenia. Further studies with more dense SNPs of the whole gene sequence for various populations will be necessary to understand the genetic contribution of DTNBP1 for the development of schizophrenia.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.neulet.2006.08.011 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Dysbindin-1 Mutation Alters Prefrontal Cortex Extracellular Glutamate and Dopamine In Vivo.
Int J Mol Sci
November 2024
Department of Psychology, Binghampton University-State University of New York, Binghampton, NY 13902, USA.
Elevated risk for schizophrenia is associated with a variation in the gene encoding dysbindin-1, which may underpin cognitive impairments in this prevalent neuropsychiatric disorder. The cognitive symptoms of schizophrenia involve anomalies in glutamate and dopamine signaling, particularly within the prefrontal cortex (PFC). Indeed, mice with mutations exhibit spatial and working memory deficits that are associated with deficits in glutamate release and NMDA receptor function as determined by slice electrophysiology.
View Article and Find Full Text PDFDNA methylation and histone modifications associated with antipsychotic treatment: a systematic review.
Mol Psychiatry
January 2025
Department of Medical Genetics, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
Antipsychotic medications are essential when treating schizophrenia spectrum and other psychotic disorders, but the efficacy and tolerability of these medications vary from person to person. This interindividual variation is likely mediated, at least in part, by epigenomic processes that have yet to be fully elucidated. Herein, we systematically identified and evaluated 65 studies that examine the influence of antipsychotic drugs on epigenomic changes, including global methylation (9 studies), genome-wide methylation (22 studies), candidate gene methylation (16 studies), and histone modification (18 studies).
View Article and Find Full Text PDFLoss of dysbindin-1 in excitatory neurons in mice impacts NMDAR-dependent behaviors, neuronal morphology and synaptic transmission in the ventral hippocampus.
Sci Rep
July 2024
Douglas Hospital Research Centre, Douglas Mental Health University Institute, 6875 LaSalle Boulevard, Montreal, QC, H4H 1R3, Canada.
Dysbindin-1, a protein encoded by the schizophrenia susceptibility gene DTNBP1, is reduced in the hippocampus of schizophrenia patients. It is expressed in various cellular populations of the brain and implicated in dopaminergic and glutamatergic transmission. To investigate the impact of reduced dysbindin-1 in excitatory cells on hippocampal-associated behaviors and synaptic transmission, we developed a conditional knockout mouse model with deletion of dysbindin-1 gene in CaMKIIα expressing cells.
View Article and Find Full Text PDFSex dimorphism controls dysbindin-related cognitive dysfunctions in mice and humans with the contribution of COMT.
Mol Psychiatry
September 2024
Department of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Cognitive dysfunctions are core-enduring symptoms of schizophrenia, with important sex-related differences. Genetic variants of the DTBPN1 gene associated with reduced dysbindin-1 protein (Dys) expression negatively impact cognitive functions in schizophrenia through a functional epistatic interaction with Catechol-O-methyltransferase (COMT). Dys is involved in the trafficking of dopaminergic receptors, crucial for prefrontal cortex (PFC) signaling regulation.
View Article and Find Full Text PDFSYMPTOM SEVERITY IN SCHIZOPHRENIA PATIENTS WITH NPAS3, DYSBINDIN-1 AND/OR TRIOBP PROTEIN PATHOLOGY IN THEIR BLOOD SERUM: A PANSS-BASED FOLLOW UP STUDY.
Psychiatr Danub
July 2023
Department of Biotechnology, University of Rijeka, Rijeka, Croatia.
Background: It has been proposed that aggregation of specific proteins in the brain may be a pathological element in schizophrenia and other chronic disorders. Multiple such aggregating proteins have now been implicated through post mortem investigation, including NPAS3 (Neuronal PAS domain protein 3), dysbindin-1 (encoded by the DTNBP1, Dystrobrevin Binding Protein 1, gene) and TRIOBP (Trio-Binding Protein, multiple isoforms). While the presence of protein aggregates in the brain is interesting in terms of understanding pathology, it is impractical as a biomarker.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!