The P2RX7 gene (coding for P2X7 purinergic receptor) has been suggested as a novel candidate gene for major depressive disorder (MDD) and bipolar disorder (BPD). The proposed risk allele (G-allele) of the rs2230912 polymorphism results in an amino acid change at the 460th position, marking this genetic variation a possibly functional one. Here we present a case-control analysis of 171 patients diagnosed with MDD or BPD and 178 controls, as well as a dimensional approach using the Hospital Anxiety and Depression Scale (HADS) for studying the Gln460Arg polymorphism of the P2RX7 gene as a genetic risk factor in depression. While case-control analysis did not show significant difference between the groups, a significant association was found between the P2RX7 polymorphism and the HADS scales in the clinical group (MANOVA P = 0.001). Both anxiety and depression scores increased as the number of G-allele increased in the genotype groups (ANOVA for HADS-anxiety: P = 0.01, HADS-depression: P < 0.001). A significant interaction of clinical status and the P2RX7 polymorphism was also found for the depression scale (MANOVA P = 0.025, subsequent ANOVA for anxiety: P = 0.252; depression: P = 0.002). Whereas patients with G-allele-present genotypes showed more elevated depression scores, level of depression in the control group was not affected by the P2RX7 genotype. In conclusion, case-control analysis did not reveal significant results, but using a symptom severity scale we could support the association between depressive disorder and the G-allele of the Gln460Arg polymorphism in the P2RX7 gene.

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Previous studies implicate involvement of dopaminergic systems in hypnotizability and report association with the COMT Val(158)Met single nucleotide polymorphism (SNP, rs4680) demonstrating the Val/Met heterozygotes as the most hypnotizable group using the Stanford Hypnotic Susceptibility Scale. This study replicates that association using an independent sample of 127 healthy Hungarian young adults and the Waterloo-Stanford Group C Scale of Hypnotic Susceptibility. Significant association (p = .016) was found between the COMT genotypes and hypnotizability, with a clear additive effect of the Val allele: Hypnotizability scores were highest in Val/Val (5.9), intermediate in Val/Met (4.7), and lowest in Met/Met (4.1). Differences between these results and those of previous studies support recent findings suggesting an inverted-U-shaped relation between dopamine level in the prefrontal cortex and cognitive functioning. The present study replicates association of COMT Val(158)Met SNP and hypnotizability and stresses the importance of mediating factors, such as group vs. individual inductions.

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Objective We aim to provide a publicly available Hungarian version of the BPAQ; compare the BPAQ factors to other personality traits; and compare both the original BPAQ factor structure provided by Buss and Perry (J. Pers. Soc. Psychol., 63, 1992, 452), the revised BPAQ‐SF factor structure by Bryant and Smith (J. Res. Pers., 35, 2001, 138), and the BAQ by Webster et al. (Aggress. Behav., 40, 2014, 120). Methods The validation of the Hungarian version of the BPAQ was carried out on a Hungarian university sample (N = 841). There were three main focuses of data analysis: descriptive statistics, correlations, and confirmatory factor analyses. Results CFA‐related statistics showed an adequate fit for the BPAQ 4 factors; however, contrary to prior validations of BPAQ, we were not able to clearly define the verbal aggression factor. We found that the shorter form of the BPAQ has a better model fit on our sample than the original form, while the model fit of the BAQ was in‐between these. BPAQ scales showed low to moderate relationship with the Barratt Impulsivity Scale and Hospital Anxiety and Depression Scale. Conclusion Both the BPAQ and the BPAQ‐SF, also the BAQ provide acceptable model fitting on a Hungarian sample of university students. While most of BPAQ items provided adequate loadings on their hypothesized factors, two items (21 and 27) did not. We argue this is the result of conceptual inaccuracy of the original items.

Altered serum levels of vascular endothelial growth factor (VEGF) and tumor necrosis factor alpha (TNFalpha) have been implicated in therapy response of depression. We analyzed effects of 4 functional SNPs of VEGF and TNF alpha genes on MDD to test their possible role in pathomechanism of MDD.We recruited 293 inpatients diagnosed for major depressive disorder (MDD) and 443 healthy volunteers. MDD was diagnosed by DSM-IV criteria and measured by Montgomery-Asberg Depression Scale (MADRS). DNA was extracted from buccal mucosa samples given by all participants. Likelihood ratio tests for case-control and mutlivariate linear analysis for quantitative phenotype models were performed in SPSS 17.0 software. We identified a protective allele against MDD as the frequency of G allele of rs1800629 (previously associated with lower TNFa serum level) was 2.7 fold higher in the control group compared to MDD group (LRT=4.197; p=0.040). Higher frequency of the same allele was found among SSRI responders compared to non-responders (LRT=6.281; p=0.012). Significant GxG interactions were shown within MDD group: epistatic effect of allele variants and also genotypes of the four investigated SNPs were significant on MADRS score (for risk alleles: p modell =0.024; p interaction =0.005; Adj.R 2 =0.259; for genotypes: p modell =0.035; p interaction =0.007; Adj.R 2 =0.371). These findings suggest that TNFalpha and VEGF genes are associated with MDD and SSRI response. Our results support the molecular crosstalk between VEGF and TNFalpha pathway by a genetic interaction.