Efficacy of Retrospective Recall of Attention-Deficit Hyperactivity Disorder Symptoms: A Twin Study

Schultz, Mark; Rabi, Keren; Faraone, Stephen V.; Kremen, William S.; Lyons, Michael J.

doi:10.1375/183242706776382374

Cited by 14 publications

(21 citation statements)

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“…Recently, four adult population twin studies using self-ratings of ADHD symptoms have been completed, which all found heritabilities that are far lower than those found in similar studies of parent- or teacher-rated cADHD: 41% for retrospectively reported childhood ADHD symptoms in a sample of 345 US veterans aged 41–58 years old, 24 40% for current inattention problems in a Dutch study of 4245 18–30-year olds, 8 30% for current ADHD symptoms in a Dutch study of over 12 000 twin pairs with an average age of 31 years 25 and 35% for current ADHD in a Swedish sample of more than 15 000 twin pairs aged 20–46 years (Larsson et al , unpublished data). The situation is similar in adolescence, as adolescent twin studies using self-ratings show lower heritability estimates than studies of parent or teacher ratings, 26, 27 suggesting that self-ratings may be a poorer measure of the underlying genetic liability to ADHD than informant reports or clinical interviews.…”

Section: Heritability Family Studies Suitability For Genetic Studiesmentioning

confidence: 93%

“…The family studies diagnosed subjects with structured interviews that evaluated childhood onset of impairing symptoms and the presence of impairment in multiple settings as required by Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. In contrast, with the exception of Schultz et al , 34 the twin studies used rating scale measures of ADHD symptoms that do not query for childhood onset and do not systematically assess impairment in multiple settings.…”

Section: Heritability Family Studies Suitability For Genetic Studiesmentioning

confidence: 99%

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The genetics of attention deficit/hyperactivity disorder in adults, a review

et al. 2011

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The adult form of attention deficit/hyperactivity disorder (aADHD) has a prevalence of up to 5% and is the most severe long-term outcome of this common neurodevelopmental disorder. Family studies in clinical samples suggest an increased familial liability for aADHD compared with childhood ADHD (cADHD), whereas twin studies based on self-rated symptoms in adult population samples show moderate heritability estimates of 30–40%. However, using multiple sources of information, the heritability of clinically diagnosed aADHD and cADHD is very similar. Results of candidate gene as well as genome-wide molecular genetic studies in aADHD samples implicate some of the same genes involved in ADHD in children, although in some cases different alleles and different genes may be responsible for adult versus childhood ADHD. Linkage studies have been successful in identifying loci for aADHD and led to the identification of LPHN3 and CDH13 as novel genes associated with ADHD across the lifespan. In addition, studies of rare genetic variants have identified probable causative mutations for aADHD. Use of endophenotypes based on neuropsychology and neuroimaging, as well as next-generation genome analysis and improved statistical and bioinformatic analysis methods hold the promise of identifying additional genetic variants involved in disease etiology. Large, international collaborations have paved the way for well-powered studies. Progress in identifying aADHD risk genes may provide us with tools for the prediction of disease progression in the clinic and better treatment, and ultimately may help to prevent persistence of ADHD into adulthood.

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Section: Heritability Family Studies Suitability For Genetic Studiesmentioning

confidence: 93%

Section: Heritability Family Studies Suitability For Genetic Studiesmentioning

confidence: 99%

The genetics of attention deficit/hyperactivity disorder in adults, a review

et al. 2011

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“…As pointed out in the introduction, different assessment procedures and verification of symptoms might impact on heritability. Several twin studies have shown that retrospective self‐ratings give a much lower heritability (32–45%) than parent or teacher ratings …”

Section: Heritability In Adhdmentioning

confidence: 99%

Recent developments in the genetics of attention‐deficit hyperactivity disorder

Grimm

Kittel‐Schneider

Reif

2018

Psychiatry Clin Neurosci

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Attention-deficit hyperactivity disorder (ADHD) is a developmental psychiatric disorder that affects children and adults. ADHD is one of the psychiatric disorders with the strongest genetic basis according to familial, twin, and single nucleotide polymorphisms (SNP)-based epidemiological studies. In this review, we provide an update of recent insights into the genetic basis of ADHD. We discuss recent progress from genome-wide association studies (GWAS) looking at common variants as well as rare copy number variations. New analysis of gene groups, so-called functional ontologies, provide some insight into the gene networks afflicted, pointing to the role of neurodevelopmentally expressed gene networks. Bioinformatic methods, such as functional enrichment analysis and protein-protein network analysis, are used to highlight biological processes of likely relevance to the etiology of ADHD. Additionally, copy number variations seem to map on important pathways implicated in synaptic signaling and neurodevelopment. While some candidate gene associations of, for example, neurotransmitter receptors and signaling, have been replicated, they do not seem to explain significant variance in recent GWAS. We discuss insights from recent case-control SNP-GWAS that have presented the first whole-genome significant SNP in ADHD.

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“…Adoption studies showed that the biological parents of hyperactive children carry a higher risk for ADHD compared to adoptive parents (Cantwell 1975; Morrison and Stewart 1973), and that first-degree adoptive relatives of probands with ADHD have a lower disease risk than the first-degree biological relatives of non-adopted ADHD probands (Sprich et al 2000). More than 20 twin studies have been published in the last 32 years, most reporting estimates of heritability for ADHD between 60 and nearly 100%, with a mean of 76% (Faraone et al 2005; Haberstick et al 2008; Heiser et al 2006; McLoughlin et al 2007; Schultz et al 2006). …”

Section: Reviewmentioning

confidence: 99%

Genome-wide association studies in ADHD

2009

Self Cite

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Attention-deficit/hyperactivity disorder, ADHD, is a common and highly heritable neuropsychiatric disorder that is seen in children and adults. Although heritability is estimated at around 76%, it has been hard to find genes underlying the disorder. ADHD is a multifactorial disorder, in which many genes, all with a small effect, are thought to cause the disorder in the presence of unfavorable environmental conditions. Whole genome linkage analyses have not yet lead to the identification of genes for ADHD, and results of candidate gene-based association studies have been able to explain only a tiny part of the genetic contribution to disease, either. A novel way of performing hypothesis-free analysis of the genome suitable for the identification of disease risk genes of considerably smaller effect is the genome-wide association study (GWAS). So far, five GWAS have been performed on the diagnosis of ADHD and related phenotypes. Four of these are based on a sample set of 958 parent–child trio’s collected as part of the International Multicentre ADHD Genetics (IMAGE) study and genotyped with funds from the Genetic Association Information Network (GAIN). The other is a pooled GWAS including adult patients with ADHD and controls. None of the papers reports any associations that are formally genome-wide significant after correction for multiple testing. There is also very limited overlap between studies, apart from an association with CDH13, which is reported in three of the studies. Little evidence supports an important role for the ‘classic’ ADHD genes, with possible exceptions for SLC9A9, NOS1 and CNR1. There is extensive overlap with findings from other psychiatric disorders. Though not genome-wide significant, findings from the individual studies converge to paint an interesting picture: whereas little evidence—as yet—points to a direct involvement of neurotransmitters (at least the classic dopaminergic, noradrenergic and serotonergic pathways) or regulators of neurotransmission, some suggestions are found for involvement of ‘new’ neurotransmission and cell–cell communication systems. A potential involvement of potassium channel subunits and regulators warrants further investigation. More basic processes also seem involved in ADHD, like cell division, adhesion (especially via cadherin and integrin systems), neuronal migration, and neuronal plasticity, as well as related transcription, cell polarity and extracellular matrix regulation, and cytoskeletal remodeling processes. In conclusion, the GWAS performed so far in ADHD, though far from conclusive, provide a first glimpse at genes for the disorder. Many more (much larger studies) will be needed. For this, collaboration between researchers as well as standardized protocols for phenotyping and DNA-collection will become increasingly important.

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Efficacy of Retrospective Recall of Attention-Deficit Hyperactivity Disorder Symptoms: A Twin Study

Cited by 14 publications

References 58 publications

The genetics of attention deficit/hyperactivity disorder in adults, a review

The genetics of attention deficit/hyperactivity disorder in adults, a review

Recent developments in the genetics of attention‐deficit hyperactivity disorder

Genome-wide association studies in ADHD

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