Associations between LSAMP gene polymorphisms and major depressive disorder and panic disorder

The purpose of this case–control genetic association study was to explore potential relationships between polymorphisms in the limbic system-associated membrane protein (LSAMP) gene and mood and anxiety disorders. A total of 21 single-nucleotide polymorphisms (SNPs) from the LSAMP gene were analyzed in 591 unrelated patients with the diagnoses of major depressive disorder (MDD) or panic disorder (PD) and in 384 healthy control subjects. The results showed a strong association between LSAMP SNPs and MDD, and a suggestive association between LSAMP SNPs and PD. This is the first evidence of a possible role of LSAMP gene in mood and anxiety disorders in humans

Analysis of SNP profiles in patients with major depressive disorder

The present study focused on 91 single-nucleotide polymorphisms (SNPs) in 21 candidate genes to find associations with major depressive disorder (MDD). In total, 160 healthy controls and 177 patients with MDD were studied. We applied arrayed primer extension (APEX) based genotyping technology followed by association and haplotype analysis. SNPs in CCKAR, DRD1, DRD2, and HTR2C genes showed nominally significant associations with MDD. None of these associations remained significant after adjustment for multiple testing. Haplotype analysis revealed CCKAR haplotypes to be associated with MDD (global p=0.004). More precisely, we found the GAGT haplotype to be associated with increased risk for MDD (OR 7.42, 95% CI 2.13–25.85, p=0.002). This haplotype effect remained significant after Bonferroni correction (p=0.04 after Bonferroni's adjustment). Altogether we were able to find some nominal associations, but due to small sample size these results should be taken as exploratory. However, the effect of GAGT haplotype on the CCKAR gene may be considered as increasing the risk for MDD

Association analysis of limbic system-associated membrane protein gene polymorphisms in mood and anxiety disorders

Poster abstrac

Increased cannabis intake during the COVID-19 pandemic is associated with worsening of depression symptoms in people with PTSD.

BACKGROUND: Some evidence suggests substance use affects clinical outcomes in people with posttraumatic stress disorder (PTSD). However, more work is required to examine links between mental health and cannabis use in PTSD during exposure to external stressors such as the COVID-19 pandemic. This study assessed mental health factors in individuals with self-reported PTSD to: (a) determine whether stress, anxiety, and depression symptoms were associated with changes in cannabis consumption across the pandemic, and (b) to contrast the degree to which clinically significant perceived symptom worsening was associated with changes in cannabis intake. METHOD: Data were obtained as part of a larger web-based population survey from April 3rd to June 24th 2020 (i.e., first wave of the pandemic in Canada). Participants (N = 462) with self-reported PTSD completed questionnaires to assess mental health symptoms and answered questions pertaining to their cannabis intake. Participants were categorized according to whether they were using cannabis or not, and if using, whether their use frequency increased, decreased, or remained unchanged during the pandemic. RESULTS: Findings indicated an overall perceived worsening of stress, anxiety, and depression symptoms across all groups. A higher-than-expected proportion of individuals who increased their cannabis consumption reached threshold for minimal clinically important worsening of depression, X(3) = 10.795, p = 0.013 (Cramer's V = 0.166). CONCLUSION: Overall, those who increased cannabis use during the pandemic were more prone to undergo meaningful perceived worsening of depression symptoms. Prospective investigations will be critical next steps to determine the directionality of the relationship between cannabis and depressive symptoms

Polymorphisms in wolframin (WFS1) gene are possibly related to increased risk for mood disorders

Wolfram syndrome gene (WFS1) has been suggested to have a role in the susceptibility for mood disorders. A 26-fold increased risk for psychiatric disorders in WFS1 mutation carriers has been suggested. In this study we tested the hypothesis that the WFS1 gene is related to the risk for mood disorders. We analysed 28 single-nucleotide polymorphisms (SNPs) of the WFS1 gene in 224 unrelated patients with major depressive disorder and bipolar disorder and in 160 healthy control subjects. Patients were further stratified according to their comorbidity with anxiety disorders. We applied arrayed primer extension (APEX)-based genotyping technology followed by association and haplotype analysis. Five SNPs in the WFS1 gene were associated with major depressive disorder, and three SNPs with bipolar disorder. Haplotype analysis revealed a common GTA haplotype, formed by SNPs 684C/G, 1185C/T and 1832G/A, conferring risk for affective disorders. Specifically, for major depression the GTA haplotype has an OR of 1.59 (p=0.01) and for bipolar disorder an OR of 1.89 (p=0.03). These results support the hypothesis that the WFS1 gene is involved in the genetic predisposition for mood disorders

Association study of 90 candidate gene polymorphisms in panic disorder

Objective In the present investigation we screened a large number of single nucleotide polymorphisms in the genes relevant to the neurobiology of anxiety for their association with panic disorder (PD). Methods The study sample included 127 patients with PD and 146 healthy control subjects. Using Arrayed Primer Extension technology we genotyped 90 polymorphisms in 21 candidate genes of serotonin, cholecystokinin, dopamine and opioid neurotransmitter systems. The association and haplotype analyses were performed in the whole group (PD-all) and in the subgroups of PD comorbid with major depression (PD-comorbid, n=60) and without any comorbidity (PD-pure, n=42). Results From the set of 90 polymorphisms, eight single nucleotide polymorphism markers in eight genes displayed at least a nominal association with any of the studied PD phenotype subgroups. Several polymorphisms of cholecystokinin, serotonin and dopamine systems were associated with PD-all and/or PD-comorbid phenotypes, while pure PD was associated only with HTR2A receptor 102T-C (P=0.01) and DRD1 receptor −94G-A (P=0.02) polymorphisms. Haplotype analysis supported an association of the cholecystokinin gene TG haplotype with the PD-all group (P=0.04), whereas DRD1 receptor CAA and HTR2A receptor AT haplotypes were associated with a lower risk for PD-pure phenotype (P=0.03 and P=0.04, respectively). Conclusions The study results suggest that genetic variants of several candidate genes of neurotransmitter systems, each of a minor individual effect, may contribute to the susceptibility to PD. Our data also indicate that genetic variability may have a distinctive influence on pure and comorbid phenotypes of PD

P.3.031 Association study of 90 candidate genetic polymorphisms in panic disorder: Positive findings with SNPs in serotonin, cholecystokinin and dopamine related genes

Poster session: Anxiety disorder and anxiolyti

P.3.05 Association and haplotype analaysis of 90 single-nucleotide polymorphisms in mood disorders

Abstract of the ECNP Workshop on Neuropsychopharmacology for Young Scientists in Europe Nice, France March 3–6, 200