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Analysis of association between LPHN3 markers and substance use disorder

ABSTRACT: Analysis of association between LPHN3 markers and substance use disorder

PROVIDER: PRJNA448611 | ENA |

REPOSITORIES: ENA

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Analysis of association between LPHN3 markers and substance use disorder

Project description:Genetic factors are strongly implicated in the susceptibility to develop externalizing syndromes such as attention deficit/hyperactivity disorder (ADHD), oppositional defiant disorder, conduct disorder, and substance use disorder (SUD). Variants in the ADGRL3 (LPHN3) gene predispose to ADHD and predict ADHD severity, disruptive behaviors comorbidity, long-term outcome, and response to treatment. In this study, we investigated whether variants within ADGRL3 are associated with SUD, a disorder that is frequently co-morbid with ADHD. Using family-based, case-control, and longitudinal samples from disparate regions of the world, recruited either for clinical, genetic epidemiological or pharmacogenomic studies of ADHD, we assembled recursive-partitioning frameworks (classification tree analyses) with clinical, demographic, and ADGRL3 genetic information to predict SUD susceptibility. Our results indicate that SUD can be efficiently and robustly predicted in ADHD participants. The genetic models used remained highly efficient in predicting SUD in a large sample of individuals with severe SUD from a psychiatric institution that were not ascertained on the basis of ADHD diagnosis, thus identifying ADGRL3 as a risk gene for SUD. Recursive partitioning analyses revealed that rs4860437 was the predominant predictive variant. This new methodological approach offers novel insights into higher order predictive interactions and offers a unique opportunity for translational application in the clinical assessment of patients at high risk for SUD

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Project description:Alcohol use disorder (AUD) has a profound public health impact and understanding of the molecular mechanisms underlying the development and progression of AUD remain limited. Many genetic risk loci have been identified for AUD or alcohol consumption, though the neurobiological mechanisms underlying these loci remain largely unknown. DNA methylation (DNAm) differences between individuals with and without AUD can provide insight into the mechanisms that predispose to AUD and consequences of AUD itself. Here, we provide Illumina HumanMethylation EPIC array data generated in nucleus accumbens and dorsolateral prefrontal cortex, both addiction relevant brain tissues, from 119 decedents of European ancestry: 61 controls and 58 cases. From these data we have conducted an epigenome-wide association study (EWAS) and identified several CpG associations with AUD. A subset of the identified CpGs map to genes that were previoulsy identified as associated with substance use behaviors in genetic studies, but the other CpGs map to genes previoulsy unassociated with substance use behaviors and are novel.

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