Disorder-specific genetic factors in obsessive-compulsive disorder: A comprehensive meta-analysis

This study simultaneously assessed the inter-rater reliability of the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders Axis I (SCID I) and Axis II disorders (SCID II) in a mixed sample of n = 151 inpatients and outpatients, and non-patient controls. Audiotaped interviews were assessed by independent second raters blind for the first raters' scores and diagnoses. Categorical inter-rater reliability was assessed for 12 Axis I disorders of SCID I, while both categorical and dimensional inter-rater reliability was tested for all Axis II disorders. Results revealed moderate to excellent inter-rater agreement of the Axis I disorders, while most categorically and dimensionally measured personality disorders showed excellent inter-rater agreement. Copyright © 2010 John Wiley & Sons, Ltd.

Quantitative genetic studies (i.e., twin and adoption studies) suggest that genetic influences contribute substantially to the development of attention deficit hyperactivity disorder (ADHD). Over the past 15 years, considerable efforts have been made to identify genes involved in the etiology of this disorder resulting in a large and often conflicting literature of candidate gene associations for ADHD. The first aim of the present study was to conduct a comprehensive meta-analytic review of this literature to determine which candidate genes show consistent evidence of association with childhood ADHD across studies. The second aim was to test for heterogeneity across studies in the effect sizes for each candidate gene as its presence might suggest moderating variables that could explain inconsistent results. Significant associations were identified for several candidate genes including DAT1, DRD4, DRD5, 5HTT, HTR1B, and SNAP25. Further, significant heterogeneity was observed for the associations between ADHD and DAT1, DRD4, DRD5, DBH, ADRA2A, 5HTT, TPH2, MAOA, and SNAP25, suggesting that future studies should explore potential moderators of these associations (e.g., ADHD subtype diagnoses, gender, exposure to environmental risk factors). We conclude with a discussion of these findings in relation to emerging themes relevant to future studies of the genetics of ADHD.