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      Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder

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          Abstract

          Attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are both highly heritable neurodevelopmental disorders. Evidence indicates both disorders co-occur with a high frequency, in 20–50% of children with ADHD meeting criteria for ASD and in 30-80% of ASD children meeting criteria for ADHD. This review will provide an overview on all available studies [family based, twin, candidate gene, linkage, and genome wide association (GWA) studies] shedding light on the role of shared genetic underpinnings of ADHD and ASD. It is concluded that family and twin studies do provide support for the hypothesis that ADHD and ASD originate from partly similar familial/genetic factors. Only a few candidate gene studies, linkage studies and GWA studies have specifically addressed this co-occurrence, pinpointing to some promising pleiotropic genes, loci and single nucleotide polymorphisms (SNPs), but the research field is in urgent need for better designed and powered studies to tackle this complex issue. We propose that future studies examining shared familial etiological factors for ADHD and ASD use a family-based design in which the same phenotypic (ADHD and ASD), candidate endophenotypic, and environmental measurements are obtained from all family members. Multivariate multi-level models are probably best suited for the statistical analysis.

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          Most cited references 93

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          Strong association of de novo copy number mutations with autism.

          We tested the hypothesis that de novo copy number variation (CNV) is associated with autism spectrum disorders (ASDs). We performed comparative genomic hybridization (CGH) on the genomic DNA of patients and unaffected subjects to detect copy number variants not present in their respective parents. Candidate genomic regions were validated by higher-resolution CGH, paternity testing, cytogenetics, fluorescence in situ hybridization, and microsatellite genotyping. Confirmed de novo CNVs were significantly associated with autism (P = 0.0005). Such CNVs were identified in 12 out of 118 (10%) of patients with sporadic autism, in 2 out of 77 (3%) of patients with an affected first-degree relative, and in 2 out of 196 (1%) of controls. Most de novo CNVs were smaller than microscopic resolution. Affected genomic regions were highly heterogeneous and included mutations of single genes. These findings establish de novo germline mutation as a more significant risk factor for ASD than previously recognized.
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            Psychiatric disorders in children with autism spectrum disorders: prevalence, comorbidity, and associated factors in a population-derived sample.

            Autism spectrum disorders are now recognized to occur in up to 1% of the population and to be a major public health concern because of their early onset, lifelong persistence, and high levels of associated impairment. Little is known about the associated psychiatric disorders that may contribute to impairment. We identify the rates and type of psychiatric comorbidity associated with ASDs and explore the associations with variables identified as risk factors for child psychiatric disorders. A subgroup of 112 ten- to 14-year old children from a population-derived cohort was assessed for other child psychiatric disorders (3 months' prevalence) through parent interview using the Child and Adolescent Psychiatric Assessment. DSM-IV diagnoses for childhood anxiety disorders, depressive disorders, oppositional defiant and conduct disorders, attention-deficit/hyperactivity disorder, tic disorders, trichotillomania, enuresis, and encopresis were identified. Seventy percent of participants had at least one comorbid disorder and 41% had two or more. The most common diagnoses were social anxiety disorder (29.2%, 95% confidence interval [CI)] 13.2-45.1), attention-deficit/hyperactivity disorder (28.2%, 95% CI 13.3-43.0), and oppositional defiant disorder (28.1%, 95% CI 13.9-42.2). Of those with attention-deficit/hyperactivity disorder, 84% received a second comorbid diagnosis. There were few associations between putative risk factors and psychiatric disorder. Psychiatric disorders are common and frequently multiple in children with autism spectrum disorders. They may provide targets for intervention and should be routinely evaluated in the clinical assessment of this group.
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              Personal genomes: The case of the missing heritability.

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                Author and article information

                Affiliations
                [1 ]Department of Psychiatry, Donders Institute for Brain, Cognition and Behavior, Radboud University Nijmegen Medical Center, Reinier Postlaan 10, 6525 GC Nijmegen, The Netherlands
                [2 ]Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, The Netherlands
                [3 ]Department of Human Genetics, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands
                [4 ]Department of Psychonomics, University of Amsterdam, Amsterdam, The Netherlands
                [5 ]Dr Leo Kannerhuis, Amsterdam Clinic, Amsterdam, The Netherlands
                [6 ]Department of Psychiatry, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
                Contributors
                +31-24-3512222 , +31-24-3512211 , n.lambregts-rommelse@psy.umcn.nl , j.buitelaar@psy.umcn.nl
                Journal
                Eur Child Adolesc Psychiatry
                European Child & Adolescent Psychiatry
                Springer-Verlag (Berlin/Heidelberg )
                1018-8827
                1435-165X
                11 February 2010
                11 February 2010
                March 2010
                : 19
                : 3
                : 281-295
                2839489
                20148275
                92
                10.1007/s00787-010-0092-x
                © The Author(s) 2010
                Categories
                Review
                Custom metadata
                © Springer-Verlag 2010

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