Obsessive-compulsive disorder and related symptoms amidst the COVID-19 outbreak: Results from the COLLATE project.
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ABSTRACT:
SUBMITTER: Toh WL
PROVIDER: S-EPMC8013877 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Neurogenetics of Obsessive-Compulsive Disorder
| PRJNA588485 | ENA
Project description:Neurogenetics of Obsessive-Compulsive Disorder
| PRJNA588486 | ENA
Project description:Obsessive-compulsive symptoms (OCS) in the population have been linked to obsessive-compulsive disorder (OCD) in genetic and epidemiological studies. Insulin signaling has been implicated in OCD. We extend previous work by assessing genetic overlap between OCD, population-based OCS, and central nervous system (CNS) and peripheral insulin signaling. We conducted genome-wide association studies (GWASs) in the population-based Philadelphia Neurodevelopmental Cohort (PNC, 650 children and adolescents) of the total OCS score and six OCS factors from an exploratory factor analysis of 22 questions. Subsequently, we performed polygenic risk score (PRS)-based analysis to assess shared genetic etiologies between clinical OCD (using GWAS data from the Psychiatric Genomics Consortium), the total OCS score and OCS factors. We then performed gene-set analyses with a set of OCD-linked genes centered around CNS insulin-regulated synaptic function and PRS-based analyses for five peripheral insulin signaling-related traits. For validation purposes, we explored data from the independent Spit for Science population cohort (5,047 children and adolescents). In the PNC, we found a significant shared genetic etiology between OCD and 'guilty taboo thoughts'. In the Spit for Science cohort, we additionally observed genetic sharing between 'symmetry/counting/ordering' and 'contamination/cleaning'. The CNS insulin-linked gene-set also associated with 'symmetry/counting/ordering' in the PNC. Further, we identified genetic sharing between peripheral insulin signaling-related traits: type 2 diabetes with 'aggressive taboo thoughts', and levels of fasting insulin and 2?h glucose with OCD. In conclusion, OCD, OCS in the population and insulin-related traits share genetic risk factors, indicating a common etiological mechanism underlying somatic and psychiatric disorders.
| S-EPMC7186226 | biostudies-literature
Project description:We investigated whether obsessive-compulsive (OC) symptoms from a population-based sample could be analyzed to detect genetic variants influencing obsessive-compulsive disorder (OCD). We performed a genome-wide association studies (GWAS) on the obsession (rumination and impulsions) and compulsion (checking, washing, and ordering/precision) subscales of an abbreviated version of the Padua Inventory (N = 8,267 with genome-wide genotyping and phenotyping). The compulsion subscale showed a substantial and significant positive genetic correlation with an OCD case-control GWAS (r G = 0.61, p = .017) previously published by the Psychiatric Genomics Consortium (PGC-OCD). The obsession subscale and the total Padua score showed no significant genetic correlations (r G = -0.02 and r G = 0.42, respectively). A meta-analysis of the compulsive symptoms GWAS with the PGC-OCD revealed no genome-wide significant Single-Nucleotide Polymorphisms (SNPs combined N = 17,992, indicating that the power is still low for individual SNP effects). A gene-based association analysis, however, yielded two novel genes (WDR7 and ADCK1). The top 250 genes in the gene-based test also showed a significant increase in enrichment for psychiatric and brain-expressed genes. S-Predixcan testing showed that for genes expressed in hippocampus, amygdala, and caudate nucleus significance increased in the meta-analysis with compulsive symptoms compared to the original PGC-OCD GWAS. Thus, the inclusion of dimensional symptom data in genome-wide association on clinical case-control GWAS of OCD may be useful to find genes for OCD if the data are based on quantitative indices of compulsive behavior. SNP-level power increases were limited, but aggregate, gene-level analyses showed increased enrichment for brain-expressed genes related to psychiatric disorders, and increased association with gene expression in brain tissues with known emotional, reward processing, memory, and fear-formation functions.
| S-EPMC7317414 | biostudies-literature
Project description:ObjectiveIn this study, it is aimed to determine obsessive compulsive-related disorders (OCRDs) comorbidity among the patients with obsessive compulsive disorder (OCD) and compare patients with OCD with or without comorbid OCRDs in terms of the severity of their OCD symptoms, symptom dimensions, and comorbidity with other axis I disorders.MethodsThe study included 90 patients diagnosed as having OCD according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR). The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic criteria for OCRDs were used to determine the presence of OCRDs. In order to determine the symptom dimensions and severity of these individuals' OCD symptoms, we administered the Dimensional Obsessive Compulsive Scale (DOCS) and The Yale-Brown Obsessive Compulsive Scale (Y-BOCS).ResultsIn our study, 20% of the patients with OCD simultaneously met the criteria for at least one OCRD, we also found that a significantly greater proportion of this group were men. None of the mentioned disorders was associated with any symptom dimensions we evaluated using DOCS. In addition, no differences were found in the severity of OCD symptoms and comorbid axis I disorders between the group with comorbid OCRDs and the group without comorbid OCRDs.DiscussionThere was no significant relationship between the symptom dimensions of OCD and OCRDs. It is found that OCRD comorbidity does not increase the severity of OCD symptoms and the prevalence of an axis I diagnosis.
| S-EPMC6611656 | biostudies-literature
Project description:BACKGROUND:Obsessive-compulsive disorder (OCD) is common in patients with eating disorders (EDs). There is a lack of research investigating the presence of ED symptoms among patients with OCD, despite concerns that many of these patients may be at high risk for EDs. Our objective was to assess the presence of ED symptoms in patients receiving treatment for OCD. METHODS:Adult patients with OCD (n = 132, 71% females) and controls (n = 260, 90% females) completed the Eating Disorder Examination-Questionnaire (EDE-Q) at admission to a specialized OCD outpatient unit. A small subset of patients (n = 22) also completed the EDE-Q 3-months after end of treatment. RESULTS:At the group-level, mean EDE-Q scores did not differ significantly between female patients and controls. However, female patients compared to controls were significantly more likely to score above the EDE-Q cut-off (23% vs. 11%) and have a probable ED (9% vs. 1%), indicating elevated rates of ED symptoms in the clinical range. There was no evidence of elevated rates of ED symptoms in male patients, though sample sizes were small. Preliminary follow-up data showed that certain ED symptoms improved significantly from admission to 3-month follow-up. CONCLUSIONS:Our findings suggest that while ED symptoms are not generally elevated in female patients with OCD, a considerable subset of female patients may have a clinical ED or be at high risk of developing one. Clinicians should be alert to ED symptoms in female patients with OCD, and our findings raise the issue of whether ED screening of female patients with OCD is warranted.
| S-EPMC6993325 | biostudies-literature
Project description:Obsessive-compulsive disorder (OCD) is a highly prevalent and chronic condition that is associated with substantial global disability. OCD is the key example of the 'obsessive-compulsive and related disorders', a group of conditions which are now classified together in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, and the International Classification of Diseases, 11th Revision, and which are often underdiagnosed and undertreated. In addition, OCD is an important example of a neuropsychiatric disorder in which rigorous research on phenomenology, psychobiology, pharmacotherapy and psychotherapy has contributed to better recognition, assessment and outcomes. Although OCD is a relatively homogenous disorder with similar symptom dimensions globally, individualized assessment of symptoms, the degree of insight, and the extent of comorbidity is needed. Several neurobiological mechanisms underlying OCD have been identified, including specific brain circuits that underpin OCD. In addition, laboratory models have demonstrated how cellular and molecular dysfunction underpins repetitive stereotyped behaviours, and the genetic architecture of OCD is increasingly understood. Effective treatments for OCD include serotonin reuptake inhibitors and cognitive-behavioural therapy, and neurosurgery for those with intractable symptoms. Integration of global mental health and translational neuroscience approaches could further advance knowledge on OCD and improve clinical outcomes.
| S-EPMC7370844 | biostudies-literature
Project description:Twin and family studies support a significant genetic contribution to obsessive-compulsive disorder (OCD) and related disorders, such as chronic tic disorders, trichotillomania, skin-picking disorder, body dysmorphic disorder, and hoarding disorder. Recently, population-based studies and novel laboratory-based methods have confirmed substantial heritability in OCD. Genome-wide association studies and candidate gene association studies have provided information on specific gene variations that may be involved in the pathobiology of OCD, though a substantial portion of the genetic risk architecture remains unknown.
| S-EPMC4143777 | biostudies-literature
Project description:ObjectiveIn obsessive-compulsive disorder (OCD), symmetry-related symptoms may be important. Although clinical correlates of symmetry-related symptoms have been identified in OCD, few data exist on genetic associations. Animal studies indicate involvement of dopamine in symmetry-related behavior, suggesting this may be relevant to analogous symptoms in OCD. Alterations in dopamine may also reflect environmental influences. However, the association of symmetry-related symptomatology, early adversity, and polymorphisms in dopaminergic genes has not been investigated in OCD.MethodsClinical information and polymorphisms in key dopaminergic genes were compared between OCD patients with primary symmetry symptoms and those without.ResultsOCD patients with primary symmetry symptoms comprised 46.6% (n=210) of the sample (n=451), and were older (p < 0.01), had longer illness duration (p < 0.01), higher OCD severity scores (p = 0.01), and greater comorbidity (p < 0.01) than those without. In Caucasians (n=343), genotype frequency differed significantly between groups for ANKK1 rs1800497, with more OCD patients with symmetry symptoms being homozygous for the A2 (CC) genotype (χ2 = 7.296; p = 0.026).ConclusionSymmetry symptoms have some distinct clinical features and may represent a marker of severity in OCD. However, clinical associations, in combination with the association found with the ANKK1 rs1800497 A2 variant, suggest that primary symmetry symptoms may represent a distinctive clinical and psychobiological profile.
| S-EPMC7115475 | biostudies-literature
Project description:For women with obsessive-compulsive personality disorder (OCPD) trait symptoms, coping with childbearing and parenting could be associated with postpartum depressive symptoms. Therefore, the possible relationship between OCPD trait symptoms and trajectories of postpartum depressive symptoms was examined. A cohort of 1427 women was followed from late pregnancy until 12 months' postpartum. Trajectories of postpartum depressive symptoms were determined using growth mixture modeling with five repeated assessments. Next, the relationship between OCPD trait symptoms and these trajectories was examined through multinomial regression. Three postpartum depressive symptom trajectories were identified: (1) low symptoms (92%), (2) increasing-decreasing symptoms (inverted u-shape) (5%), and (3) increasing symptoms (3%). OCPD trait symptoms were associated with a higher likelihood of the trajectories increasing-decreasing symptoms (OR 1.26; 95% CI 1.14-1.39) and increasing symptoms (OR 1.16; 95% CI 1.02-1.32), compared to reference trajectory (low symptoms), adjusted for age, educational level, unplanned pregnancy, previous depressive episode (s), and parity.
| S-EPMC6647494 | biostudies-literature