Phenotypic and genetic correlations between evoked EEG/ERP measures during the response anticipation period of a delayed response task

Smit, Dirk J.A.; Posthuma, Daniëlle; Boomsma, Dorret I.; Geus, Eco J. C. de

doi:10.1111/j.1469-8986.2008.00777.x

Cited by 7 publications

(4 citation statements)

References 62 publications

(120 reference statements)

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“…Therefore, the findings suggest that LRTC may prove useful for studying deviance from normal development, neurodevelopmental disorders such as ADHD and schizophrenia. In addition, we speculate that the developmental increases in LRTC observed during adolescence and early adulthood are related to the maturation of different cognitive functions, such as the ability to sustain attention and maintain information in working memory (Smit et al, 2009). Future research may address these issues.…”

Section: Increased Spatial Uniformity Of Lrtc May Reflect Developmentmentioning

confidence: 99%

Scale-Free Modulation of Resting-State Neuronal Oscillations Reflects Prolonged Brain Maturation in Humans

Smit¹,

Geus²,

Nieuwenhuijzen³

et al. 2011

J. Neurosci.

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Human neuronal circuits undergo life-long functional reorganization with profound effects on cognition and behavior. Well documented prolonged development of anatomical brain structures includes white and gray matter changes that continue into the third decade of life. We investigated resting-state EEG oscillations in 1433 subjects from 5 to 71 years. Neuronal oscillations exhibit scale-free amplitude modulation as reflected in power-law decay of autocorrelations-also known as long-range temporal correlations (LRTC)-which was assessed by detrended fluctuation analysis. We observed pronounced increases in LRTC from childhood to adolescence, during adolescence, and even into early adulthood (ϳ25 years of age) after which the temporal structure stabilized. A principal component analysis of the spatial distribution of LRTC revealed increasingly uniform scores across the scalp. Together, these findings indicate that the scale-free modulation of resting-state oscillations reflects brain maturation, and suggests that scaling analysis may prove useful as a biomarker of pathophysiology in neurodevelopmental disorders such as attention deficit hyperactivity disorder and schizophrenia.

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Section: Increased Spatial Uniformity Of Lrtc May Reflect Developmentmentioning

confidence: 99%

Scale-Free Modulation of Resting-State Neuronal Oscillations Reflects Prolonged Brain Maturation in Humans

Smit¹,

Geus²,

Nieuwenhuijzen³

et al. 2011

J. Neurosci.

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“…Slow-cortical potentials such as the CNV demonstrate heritability between 30% and 43% (Ref. 169). These ERP components therefore appear to index genetically influenced neural processes that are important for cognitive control.…”

Section: Quantitative Eegmentioning

confidence: 99%

Electrophysiological markers of genetic risk for attention deficit hyperactivity disorder

Tye

McLoughlin

Kuntsi

et al. 2011

Expert Rev. Mol. Med.

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Electroencephalography (EEG) is an ideal neuroscientific approach, providing a direct measurement of neural activity that demonstrates reliability, developmental stability and high heritability. This systematic review of a subset of domains evaluates the utility of electrophysiological measures as potential intermediate phenotypes for ADHD in the domains of quantitative EEG indices of arousal and intra-individual variability, and functional investigations of inhibitory and error processing using the event-related potential (ERP) technique. Each domain demonstrates consistent and meaningful associations with ADHD, a degree of genetic overlap with ADHD and potential links to specific genetic variants. Investigations of the genetic and environmental contributions to EEG/ERP and shared genetic overlap with ADHD may enhance molecular genetic studies and provide novel insights into aetiology. Such research will aid in the precise characterisation of the clinical deficits seen in ADHD and guide the development of novel intervention and prevention strategies for those at risk. KeywordsADHD; arousal; default-mode; electrophysiology; endophenotype; executive function; genetics; heritability Attention deficit hyperactivity disorder (ADHD) is a developmental condition characterised by impairing levels of inattentive, impulsive and hyperactive symptoms (Ref. 1), with prevalence in school-aged children around 5% (Ref. 2). The disorder frequently persists into adult life, with approximately 15% of children with ADHD retaining the diagnosis by the age of 25 years and a further 50% showing persistence of some symptoms giving rise to continued impairments (Ref. 3).ADHD tends to run in families, with a risk of ADHD to first-degree relatives of an affected proband around four to ten times the general population rate (Ref. 4). Twin studies suggest that around 70-80% of the phenotypic variance is explained by genetic factors (Ref. 5). Such quantitative genetic studies suggest that ADHD represents the extreme of one or more continuously distributed traits, rather than a distinct categorical disorder (Ref. 6,7,8,9,10).The conceptualisation of ADHD symptoms as continuous traits (Ref. 10) seems to better reflect the underlying aetiological processes involved, in which risk factors for ADHD influence levels of ADHD symptoms throughout the population (Ref. 8 Europe PMC Funders GroupAuthor Manuscript Expert Rev Mol Med. Author manuscript; available in PMC 2014 June 03. Published in final edited form as:Expert Rev Mol Med. ; 13: e9. doi:10.1017/S1462399411001797. Europe PMC Funders Author ManuscriptsEurope PMC Funders Author Manuscripts quantitative genetic studies support the use of both categorical and quantitative trait locus (QTL) approaches in the investigation of genetic risk factors for ADHD (Ref. 11) and the underlying neurobiological processes involved.Candidate gene studies implicate genetic variants involved in the regulation of dopamine and related neurotransmitter systems, predicted by the effects of stimulant medicatio...

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“…Data in adults (ages 18–28) point towards heritabilities of ~.50–60 for P3 and N2 amplitudes [47], with such magnitudes staying relatively stable across adulthood (ages 17–23) [48] and across early adolescence (ages 12–16) [49]. There is also evidence for the heritability of CNV in delayed response tasks (with estimates between ~.21 to ~.43, varying depending on task-load conditions and the channels considered; [50]). Nevertheless, these heritability estimates have been derived from heterogeneous paradigms, and heritability estimates on ERPs directly derived from CPTs are lacking.…”

Section: Introductionmentioning

confidence: 99%

No evidence of associations between ADHD and event-related brain potentials from a continuous performance task in a population-based sample of adolescent twins

Lau‐Zhu¹,

Tye²,

Rijsdijk³

et al. 2019

PLoS ONE

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We investigated key event-related brain potential markers (ERPs) derived from a flanked continuous performance task (CPT) and whether these would show phenotypic associations with ADHD (attention-deficit/hyperactivity disorder) in a population-based sample. We further explored whether there was preliminary evidence that such ERPs could also index genetic risk for ADHD (depending on finding phenotypic associations). Sixty-seven male-only twin pairs (N = 134; aged 12–15) from a subsample of the Twins’ Early Development Study, concordant and discordant for ADHD symptoms, performed the flanked CPT (or CPT-OX) while electroencephalography (EEG) was recorded. ERPs were obtained for cue (P3, CNV or contingency negative variation), go (P3, N2) and nogo trials (P3, N2). We found no phenotypic associations between CPT-derived ERPs and ADHD—the sizes of the estimated phenotypic correlations were nonsignificant and very small (r’s = -.11 to .04). Twin-model fitting analyses using structural equation modelling provided preliminary evidence that some of the ERPs were heritable (with the most robust effect for go-P3 latency), but there was limited evidence of any genetic associations between ERPs and ADHD, although with the caveat that our sample was small and hence had limited power. Overall, unlike in previous research, there was no evidence of phenotypic (nor preliminary evidence for genetic) associations between ADHD and CPT-derived ERPs in this study. Hence, it may be currently premature for genetic analyses of ADHD to be guided by CPT-derived ERP parameters (unlike alternative cognitive-neurophysiological approaches which may be more promising). Further research with better-powered, population-based, genetically-informative and cross-disorder samples are required, which could be facilitated by emerging mobile EEG technologies.

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Phenotypic and genetic correlations between evoked EEG/ERP measures during the response anticipation period of a delayed response task

Cited by 7 publications

References 62 publications

Scale-Free Modulation of Resting-State Neuronal Oscillations Reflects Prolonged Brain Maturation in Humans

Scale-Free Modulation of Resting-State Neuronal Oscillations Reflects Prolonged Brain Maturation in Humans

Electrophysiological markers of genetic risk for attention deficit hyperactivity disorder

No evidence of associations between ADHD and event-related brain potentials from a continuous performance task in a population-based sample of adolescent twins

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