This data supports that reduced blood catechol-O-methyltransferase expression, which may be associated with higher dopamine level, is involved both in stress-induced and non-stress-induced schizophrenia.
These findings suggest that ZNF804A affects the resting-state functional activation by interacting with COMT, and may improve our understanding of the neurobiological effects of ZNF804A and its association with schizophrenia.
As a group, BDNF Met carriers reported greater symptoms of depression on the Personality Assessment Inventory (PAI) than those without a Met allele (p = 0.004); COMT Val carriers reported greater symptoms on the PAI Schizophrenia (p = 0.007), Antisocial Features (p = 0.04), and Alcohol Problems (p = 0.03) scales than noncarriers.
Based on these data, we investigated possible effects of the interaction between COMT Val108/158Met genotype and gender on subcortical volumes among 79 patients with schizophrenia.
These results imply that PPI might be modulated by four genotypes - COMTrs4680 (primarily in males), GRIK3 rs1027599, TCF4 rs9960767, and PRODH rs385440 - indicating a role of these gene variations in the development of early information processing deficits in schizophrenia.
In this longitudinal study, we aim to investigate the expressions of Catechol-O-methyltransferase (<i>COMT</i>), serotonin 2A receptor (<i>5-HTR2A</i>), and serotonin transporter gene (<i>SLC6A4</i>) mRNA in first-episode antipsychotic-naïve schizophrenia and to test if these mRNA expressions are associated with cognitive deficits and treatment outcomes or not.
The aim of this study was to explore the association between COMT gene polymorphisms, clinical symptoms (including cognitive function), and treatment response to antipsychotic medications in patients with schizophrenia.
Hence, we measured COMT levels in prefrontal cortex obtained postmortem from 199 subjects, some of whom had a history of schizophrenia, major depressive disorders or bipolar disorders.
In this study, the aim was to conduct a meta-analysis to achieve a pooled effect size of the association between COMT gene rs165599 SNP and schizophrenia.
Our findings suggest that COMT genotype differentially influences pathways related to cognitive performance in patients with FES versus healthy individuals, providing an important insight into schizophrenia pathophysiology.
A functional single nucleotide polymorphism (SNP) present in the catechol-O-methyltransferase (COMT) gene, Val158Met (rs4680) (Chr22: 19,963,498), is possibly related to the violent behavior of schizophrenia patients.
These findings suggest that ZNF804A affects the GMV of the prefrontal cortex by interacting with COMT, which may improve our understanding of neurobiological effect of ZNF804A and its association with schizophrenia.
Mutations in the <i>LRTOMT</i> gene, which encodes a protein with homology to the catecholamine methyltransferase COMT that is linked to schizophrenia, cause deafness.
Differential moderating effects of COMT Val/Met genotype variations may similarly influence executive functions in people with schizophrenia and comorbid AUD/SUD.
We measured COMT catalytic activity in post-mortem prefrontal cortices, striata and cerebella of schizophrenia and BD patients, as well as non-affected controls.
As impaired serotonergic and dopaminergic neurotransmission is implicated in the pathogenesis of depression and schizophrenia this study sought to investigate the putative association between several functional gene polymorphisms (SERT 5-HTTLPR, MAO-A VNTR, COMTVal158Met and DAT VNTR) and schizophrenia.