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1. Attention deficit/hyperactivity disorder children with a 7-repeat allele of the dopamine receptor D4 gene have extreme behavior but normal performance on critical neuropsychological tests of attention.

Author: Swanson, J, Oosterlaan, J, Murias, M, Schuck, S, Flodman, P, Spence, MA, Wasdell, M, Ding, Y, Chi, HC, Smith, M, Mann, M, Carlson, C, Kennedy, JL, Sergeant, JA, Leung, P, Zhang, YP, Sadeh, A, Chen, C, Whalen, CK, Babb, KA, Moyzis, R, and Posner, MI
Subjects: Chromosomes, Human, Pair 11, Humans, Receptors, Dopamine D2, Cohort Studies, Chromosome Mapping, Attention, Attention Deficit Disorder with Hyperactivity, Neuropsychological Tests, Minisatellite Repeats, Alleles, Exons, Reference Values, Child, Female, Male, Receptors, Dopamine D4, Chromosomes, Human, Pair 11, Receptors, Dopamine D2, Dopamine D4, Clinical Research, Attention Deficit Disorder, Genetics, Behavioral and Social Science, Neurosciences, Pediatric, Mental Health, Brain Disorders, dopamine receptor, allele, article, attention deficit disorder, child, disease severity, exon, gene expression, human, hyperactivity, major clinical study, neuropsychological test, prediction, priority journal, reaction time, tandem repeat
Abstract: An association of the dopamine receptor D4 (DRD4) gene located on chromosome 11p15.5 and attention deficit/hyperactivity disorder (ADHD) has been demonstrated and replicated by multiple investigators. A specific allele [the 7-repeat of a 48-bp variable number of tandem repeats (VNTR) in exon 3] has been proposed as an etiological factor in attentional deficits manifested in some children diagnosed with this disorder. In the current study, we evaluated ADHD subgroups defined by the presence or absence of the 7-repeat allele of the DRD4 gene, using neuropsychological tests with reaction time measures designed to probe attentional networks with neuroanatomical foci in D4-rich brain regions. Despite the same severity of symptoms on parent and teacher ratings for the ADHD subgroups, the average reaction times of the 7-present subgroup showed normal speed and variability of response whereas the average reaction times of the 7-absent subgroup showed the expected abnormalities (slow and variable responses). This was opposite the primary prediction of the study. The 7-present subgroup seemed to be free of some of the neuropsychological abnormalities thought to characterize ADHD.
Published: 2000

2. Attention-deficit hyperactivity disorder and hyperkinetic disorder

Author: Swanson, JM, Sergeant, JA, Taylor, E., Sonuga-Barke, Ejs, Jensen, PS, and Cantwell, DP
Published: 1998

3. Effects of transcutaneous electrical nerve stimulation on cognition, behavior, and rest-activity rhythm in children with Attention Deficit Hyperactivity Disorder, combined type

Author: Jonsdottir, S, Bouma, A, Sergeant, JA, Scherder, EJA, Bouma, J.M., Clinical Neuropsychology, Faculty of Behavioural and Social Sciences, and Clinical Psychology and Experimental Psychopathology
Subjects: Male, Child Behavior, attention deficit hyperactivity disorder (ADHD) transcutaneous electrical nerve stimulation (TENS), Audiology, law.invention, Developmental psychology, 0302 clinical medicine, Cognition, law, BRAIN, Child, actigrapby, 05 social sciences, EXECUTIVE FUNCTIONS, Neuropsychology, 050301 education, General Medicine, Executive functions, SUPRACHIASMATIC NUCLEUS, Circadian Rhythm, Transcutaneous Electric Nerve Stimulation, Female, Psychology, Motor Restlessness, RESPONSE-INHIBITION, SDG 4 - Quality Education, medicine.medical_specialty, Adolescent, Rest, Motor Activity, Transcutaneous electrical nerve stimulation, 03 medical and health sciences, children, Rating scale, mental disorders, medicine, Attention deficit hyperactivity disorder, Humans, PROTEIN-LEVELS, MEMORY, PROBABLE ALZHEIMERS-DISEASE, Actigraphy, medicine.disease, SLEEP, 030227 psychiatry, Attention Deficit Disorder with Hyperactivity, RAT, DEFICIT/HYPERACTIVITY DISORDER, rest-activity rhythm, 0503 education
Abstract: Objective. The aim of this study was to examine the effects of transcutaneous electrical nerve stimulation (TENS) on cognition, behavior, and the rest-activity rhythm in children with attention deficit hyperactivity disorder, combined type (ADHD-CT). Methods. Twenty-two children diagnosed with ADHD-CT received TENS treatment during 6 weeks, 2 times 30 min a day. Neuropsychological tests were administered to assess cognition, parent/teacher behavioral rating scales were used to measure behavior, and actigraphy was used to assess the rest-activity rhythm. Results. TENS appeared to have a moderate beneficial influence on cognitive functions that load particularly on executive function. There was also improvement in behavior as measured by parent/teacher behavioral rating scales. Moreover, motor restlessness during sleep and motor activity during the day decreased by TENS. Conclusions. The effects of TENS in children with ADHD are modest but encouraging and warrant further research. © 2004, Sage Publications. All rights reserved.
Published: 2004
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4. ERPs Associated with Anticipation and Evaluation of Monetary Reward and Punishment in Children with ADHD

Author: van Meel, CS (Catharine), Heslenfeld, DJ, Oosterlaan, J, Luman, M, Sergeant, JA, and Department of Psychology, Education and Child Studies
Subjects: behavioral disciplines and activities
Abstract: Background. Several models of attention-deficit hyperactivity disorder (ADHD) propose abnormalities in the response to behavioural contingencies. Using event-related potentials (ERPs), the present study investigated the monitoring and subsequent evaluation of performance feedback resulting in either reward or punishment in children with ADHD (N=18) and normal controls (N=18) aged 8 to 12 years. Methods. Children performed a time production task, in which visual performance feedback was given after each response. To manipulate its motivational salience, feedback was coupled with monetary gains, losses or no incentives. Results. Performance feedback signalling omitted gains as well as omitted losses evoked a feedback-related negativity (FRN) in control children. The FRN, however, was entirely absent in children with ADHD in all conditions. Moreover, while losses elicited enhanced amplitudes of the late positive potential (LPP) in controls, omitted rewards had this effect in ADHD. Conclusions. The lack of modulation of the FRN by contingencies in ADHD suggests deficient detection of environmental cues as a function of their motivational significance. LPP findings suggest diminished response to punishment, but oversensitivity to the loss of desired rewards. These findings suggest that children with ADHD have problems assigning relative motivational significance to outcomes of their actions.
Published: 2011

5. Genen en neurocognitieve vaardigheden: is er een relatie bij ADHD?

Author: Boonstra, AM, Kooij, JJS, Buitelaar, JK, Oosterlaan, J, Sergeant, JA, Heister, JGAM, Franke, B, and Department of Psychology, Education and Child Studies
Published: 2006

6. Actometrie, slaap en medicatie bij volwassenen met ADHD

Author: Boonstra, AM, Kooij, JJS, Oosterlaan, J, Sergeant, JA, Buitelaar, JK, Someren, EJW, and Department of Psychology, Education and Child Studies
Published: 2006

7. Scala di valutazione dei Comportamenti Dirompenti per insegnanti (SCOD-I)

Author: MARZOCCHI, GIAN MARCO, Oosterlaan, J, De Meo, T, Di Pietro, M, Pezzica, S, Cavolina, P, Sergeant, JA, Zuddas, A., Marzocchi, G, Oosterlaan, J, De Meo, T, Di Pietro, M, Pezzica, S, Cavolina, P, Sergeant, J, and Zuddas, A
Subjects: M-PSI/04 - PSICOLOGIA DELLO SVILUPPO E PSICOLOGIA DELL'EDUCAZIONE, Rating Scale, Disturbi di Comportamento, ADHD, ODD, CD
Published: 2001

8. Eunethydis: a statement of the ethical principles governing the relationship between the European group for ADHD guidelines, and its members, with commercial for-profit organisations

Author: Sergeant, JA, Banaschewski, T, Buitelar, J, Coghill, D, Danckaerts, M, Doepfner, M, Rothenberger, A, Santosh, P, Sonuga-Barke, EJS, Steinhausen, H-C, Taylor, E, Zuddas, A, Sergeant, JA, Banaschewski, T, Buitelar, J, Coghill, D, Danckaerts, M, Doepfner, M, Rothenberger, A, Santosh, P, Sonuga-Barke, EJS, Steinhausen, H-C, Taylor, E, and Zuddas, A
Abstract: The Eunethydis ADHD Guidelines group set out here the ethical principles governing the relationship between the group and industry. The principles set out here are provided to ensure that this is both done and seen to be done. The impetus for these guidelines comes from within the Group and is linked to the recognition for the need for an open and transparent basis for Group-industry relations, especially in the light of the present concern that the pharmaceutical industry may be exerting a growing influence on the actions of researchers and clinicians in the ADHD field.
Published: 2010

9. Contrasting deficits on Executive Functions between ADHD and Reading Disabled children

Author: Marzocchi, G, Oosterlaan, J, Zuddas, A, Cavolina, P, Geurts, H, Redigolo, D, Vio, C, Sergeant, J, MARZOCCHI, GIAN MARCO, Sergeant, JA, Marzocchi, G, Oosterlaan, J, Zuddas, A, Cavolina, P, Geurts, H, Redigolo, D, Vio, C, Sergeant, J, MARZOCCHI, GIAN MARCO, and Sergeant, JA
Abstract: Background: The object of this study was to analyze the executive functioning of children with attention deficit hyperactivity disorder (ADHD) or reading disability (RD) independent of their non-executive deficits. Methods: Three carefully diagnosed groups of children, aged between 7 and 12 years (35 ADHD, 22 RD and 30 typically developing children), were tested on a wide range of tasks related to five major domains of executive functioning (EF): inhibition, visual working memory, planning, cognitive flexibility, and verbal fluency. Additional tasks were selected for each domain to control for non-executive processing. Results: ADHD children were impaired on interference control, but not on prepotent and ongoing response suppression. ADHD showed deficits on visual working memory, planning, cognitive flexibility and phonetic fluency. RD children were impaired on phonetic fluency. The only EF measure that differentiated ADHD from RD was planning. Conclusions: The present sample of ADHD children showed several EF deficits, whereas RD children were almost spared executive dysfunction, but exhibited deficits in phonetic fluency. © 2007 The Authors.
Published: 2008

10. Factor structure and cultural aspects of Disruptive Behaviour Disorders symptoms in Italian children

Author: Zuddas, A, Marzocchi, G, Oosterlaan, J, Cavolina, P, Ancilletta, B, Sergeant, J, Sergeant, JA, MARZOCCHI, GIAN MARCO, Zuddas, A, Marzocchi, G, Oosterlaan, J, Cavolina, P, Ancilletta, B, Sergeant, J, Sergeant, JA, and MARZOCCHI, GIAN MARCO
Abstract: Objective: Poor parent and teacher awareness for attention-deficit/hyperactivity disorder (ADHD) and the scepticism of many clinicians on the prevalence of the disorder, make Italy an interesting environment in which to verify neuropsychological constructs generated in a predominantly Northern American cultural contest. The aim of the study was to verify, by factor confirmatory analysis, the empirical validity of the DSM constructs underlying the diagnostic criteria for developmental disruptive behaviour disorders in Italian school-age children. Methods: Scores for DSM-IV inattention and hyperactivity/impulsivity, for oppositional defiant disorder (ODD) and for conduct disorder (CD) symptoms in 6-12 years old Italian children were analysed from 1575 parent and 1085 teacher forms of the disruptive behaviour disorders questionnaires collected in four different Italian regions. Results: Reliability indicates high internal consistencies for both parent and teacher rating of inattention, hyperactivity/impulsivity, and oppositionality, but not for conduct problems. In accordance with the literature, a relatively low inter-rater convergent and discriminant validity correlation was observed comparing measures obtained by between parents and teachers. Confirmatory factor analysis of both parent and teacher data showed a better fit for a four-factor model, indicating a factor structure in accordance with the DSM-IV taxonomy. When completed by parents and teachers of clinically assessed ADHD, dyslexic or normal children, the disruptive behavioural disorder questionnaires showed a significant predictive diagnostic value. Conclusion: Although an informant variance higher that dimensional (trait) variance was observed, the study provides support for DSM-IV taxonomy for developmental disruptive disorders, showing construct validity of ADHD. ODD and CD could also be distinguished from each other. © 2005 Elsevier SAS. All rights reserved.
Published: 2006

11. Comportamenti di disattenzione, iperattività e oppositività secondo i genitori: un questionario per la valutazione dei comportamenti dirompenti (SCOD-G) in età evolutiva

Author: Marzocchi, G, Oosterlaan, J, De Meo, T, Di Pietro, M, Pezzica, S, Cavolina, P, Sergeant, J, Zuddas, A, MARZOCCHI, GIAN MARCO, Sergeant, JA, Zuddas, A., Marzocchi, G, Oosterlaan, J, De Meo, T, Di Pietro, M, Pezzica, S, Cavolina, P, Sergeant, J, Zuddas, A, MARZOCCHI, GIAN MARCO, Sergeant, JA, and Zuddas, A.
Published: 2003

12. Scala di valutazione dei Comportamenti Dirompenti per insegnanti (SCOD-I)

Author: Marzocchi, G, Oosterlaan, J, De Meo, T, Di Pietro, M, Pezzica, S, Cavolina, P, Sergeant, J, Zuddas, A, MARZOCCHI, GIAN MARCO, Sergeant, JA, Zuddas, A., Marzocchi, G, Oosterlaan, J, De Meo, T, Di Pietro, M, Pezzica, S, Cavolina, P, Sergeant, J, Zuddas, A, MARZOCCHI, GIAN MARCO, Sergeant, JA, and Zuddas, A.
Published: 2001

13. Psychological mechanisms of enhanced risk of addiction in children of alcoholics: a dual pathway?

Author: Wiers, RW, primary, Sergeant, JA, additional, and Gunning, WB, additional
Published: 1994
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14. Developmental trajectories of neural mechanisms supporting conflict and error processing in middle childhood.

Author: van Meel CS, Heslenfeld DJ, Rommelse NN, Oosterlaan J, and Sergeant JA
Abstract: To study age-related changes in cognitive control, event-related potentials (ERPs) of children aged 6-9 years, 10-12 years, and young adults were recorded during a Flanker task. Younger children were more susceptible to conflict than older ones and adults. The N2 in incongruent trials was smaller in younger than older children, who did not differ from adults. The error-related negativity (ERN) following errors, however, was larger in adults than in children, but did not differ between younger and older children. Delayed development of neural responses to error processing relative to conflict monitoring may indicate dissociable maturational time tables of subdivisions of the anterior cingulate cortex. [ABSTRACT FROM AUTHOR]
Published: 2012

15. International variation in treatment procedures for ADHD: social context and recent trends.

Author: Hinshaw SP, Scheffler RM, Fulton BD, Aase H, Banaschewski T, Cheng W, Mattos P, Holte A, Levy F, Sadeh A, Sergeant JA, Taylor E, Weiss MD, Hinshaw, Stephen P, Scheffler, Richard M, Fulton, Brent D, Aase, Heidi, Banaschewski, Tobias, Cheng, Wenhong, and Mattos, Paulo
Abstract: Objective: Scientific and clinical interest in attention-deficit hyperactivity disorder (ADHD) is increasing worldwide. This article presents data from a cross-national workshop and survey related to questions of variability in diagnostic and, particularly, treatment procedures.Methods: Representatives of nine nations (Australia, Brazil, Canada, China, Germany, Israel, the Netherlands, Norway, and the United Kingdom), plus the United States, who attended a 2010 workshop on ADHD, responded to a survey that addressed diagnostic procedures for ADHD; treated prevalence of medication approaches, as well as psychosocial interventions; types of medications and psychosocial treatments in use; payment systems; beliefs and values of the education system; trends related to adult ADHD; and cultural and historical attitudes and influences related to treatment.Results: Use of both medication and psychosocial treatment for ADHD varies widely within and across nations. More expensive long-acting formulations of medications are becoming more widespread. Nations with socialized medical care provide a wide array of evidence-based interventions. Economic, historical, and political forces and cultural values are related to predominant attitudes and practices. Strong antipsychiatry and antimedication voices remain influential in many nations.Conclusions: There is considerable variation in implementation of care for ADHD. Recognition of the social context of ADHD is an important step in ensuring access to evidence-based interventions for this prevalent, chronic, and impairing condition. [ABSTRACT FROM AUTHOR]
Published: 2011
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16. Pragmatics fragmented: the factor structure of the Dutch Children's Communication Checklist (CCC)

Author: Geurts HM, Hartman C, Verté S, Oosterlaan J, Roeyers H, and Sergeant JA
Abstract: Background: A number of disorders are associated with pragmatic difficulties. Instruments that can make subdivisions within the larger construct of pragmatics could be important tools for disentangling profiles of pragmatic difficulty in different disorders. The deficits underlying the observed pragmatic difficulties may be different for different disorders. Aims: To study the construct validity of a pragmatic language questionnaire. Method & Procedures: The construct of pragmatics is studied by applying exploratory factor analysis (EFA) and confirmatory factor analysis to the parent version of the Dutch Children's Communication Checklist (CCC; Bishop 1998). Parent ratings of 1589 typically developing children and 481 children with a clinical diagnosis were collected. Four different factor models derived from the original CCC scales and five different factor models based on EFA were compared with each other. The models were cross-validated. Outcomes & Results: The EFA-derived models were substantively different from the originally proposed CCC factor structure. EFA models gave a slightly better fit than the models based on the original CCC scales, though neither provided a good fit to the parent data. Coherence seemed to be part of language form and not of pragmatics, which is in line with the adaptation of the CCC, the CCC-2 (Bishop 2003). Most pragmatic items clustered together in one factor and these pragmatic items also clustered with items related to social relationships and specific interests. Conclusions & Implications: The nine scales of the original CCC do not reflect the underlying factor structure. Therefore, scale composition may be improved on and scores on subscale level need to be interpreted cautiously. Therefore, in interpreting the CCC profiles, the overall measure might be more informative than the postulated subscales as more information is needed to determine which constructs the suggested subscales are actually measuring. [ABSTRACT FROM AUTHOR]
Published: 2009
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17. Support for an independent familial segregation of executive and intelligence endophenotypes in ADHD families.

Author: Rommelse NNJ, Altink ME, Oosterlaan J, Buschgens CJM, Buitelaar J, and Sergeant JA
Abstract: BACKGROUND: Impairments in executive functioning (EF) and intelligence quotient (IQ) are frequently observed in children with attention deficit hyperactivity disorder (ADHD). The aim of this paper was twofold: first, to examine whether both domains are viable endophenotypic candidates for ADHD and second to investigate whether deficits in both domains tend to co-segregate within families. METHOD: A large family-based design was used, including 238 ADHD families (545 children) and 147 control families (271 children). Inhibition, visuospatial and verbal working memory, and performance and verbal IQ were analysed. RESULTS: Children with ADHD, and their affected and non-affected siblings were all impaired on the EF measures and verbal IQ (though unimpaired on performance IQ) and all measures correlated between siblings. Correlations and sibling cross-correlations were not significant between EF and IQ, though they were significant between the measures of one domain. Group differences on EF were not explained by group differences on IQ and vice versa. The discrepancy score between EF and IQ correlated between siblings, indicating that siblings resembled each other in their EF-IQ discrepancy instead of having generalized impairments across both domains. Siblings of probands who had an EF but not IQ impairment, showed a comparable disproportionate lower EF score in relation to IQ score. The opposite pattern was not significant. CONCLUSIONS: The results supported the viability of EF and IQ as endophenotypic candidates for ADHD. Most findings support an independent familial segregation of both domains. Within EF, similar familial factors influenced inhibition and working memory. Within IQ, similar familial factors influenced verbal and performance IQ. [ABSTRACT FROM AUTHOR]
Published: 2008
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18. The dopamine receptor D4 7-repeat allele and prenatal smoking in ADHD-affected children and their unaffected siblings: no gene--environment interaction.

Author: Altink ME, Arias-Vásquez A, Franke B, Slaats -Willemse DIE, Buschgens CJM, Rommelse NNJ, Fliers EA, Anney R, Brookes K, Chen W, Gill M, Mulligan A, Sonuga-Barke E, Thompson M, Sergeant JA, Faraone SV, Asherson P, and Buitelaar JK
Published: 2008
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19. White matter hyperintensities and working memory: an explorative study.

Author: Oosterman JM, van Harten B, Weinstein HC, Scheltens P, Sergeant JA, and Scherder EJ
Published: 2008
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20. Hyperactive night and day? Actigraphy studies in adult ADHD: a baseline comparison and the effect of methylphenidate.

Author: Boonstra AM, Kooij JJS, Oosterlaan J, Sergeant JA, Buitelaar JK, and Van Someren EJW
Published: 2007

21. Executive functioning in adult ADHD: a meta-analytic review.

Author: Boonstra AM, Oosterlaan J, Sergeant JA, and Buitelaar JK
Abstract: BACKGROUND: Several theoretical explanations of ADHD in children have focused on executive functioning as the main explanatory neuropsychological domain for the disorder. In order to establish if these theoretical accounts are supported by research data for adults with ADHD, we compared neuropsychological executive functioning and non-executive functioning between adults with ADHD and normal controls in a meta-analytic design. METHOD: We compared 13 studies that (1) included at least one executive functioning measure, (2) compared the performance of an adult ADHD group with that of an adult normal control group, (3) provided sufficient information for calculation of effect sizes, and (4) used DSM-III-R or DSM-IV criteria to diagnose ADHD. RESULTS: We found medium effect sizes both in executive functioning areas [verbal fluency (d= 0-62), inhibition (d = 0-64 and d = 0.89), and set shifting (d = 0.65)] and in non-executive functioning domains [consistency of response (d = 0.57), word reading (d = 0.60) and color naming (d = 0.62)]. CONCLUSIONS: Neuropsychological difficulties in adult ADHD may not be confined to executive functioning. The field is in urgent need of better-designed executive functioning tests, methodological improvements, and direct comparisons with multiple clinical groups to answer questions of specificity. [ABSTRACT FROM AUTHOR]
Published: 2005
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22. Peripheral electrical stimulation in Alzheimer's disease: a randomized controlled trial on congestion and behavior.

Author: van Dijk KRA, Scheltens P, Luijpen MW, Sergeant JA, and Scherder EJA
Abstract: In a number of studies, peripheral electrical nerve stimulation has been applied to Alzheimer's disease (AD) patients who lived in a nursing home. Improvements were observed in memory, verbal fluency, affective behavior, activities of daily living and on the rest-activity rhythm and pupillary light reflex. The aim of the present, randomized, placebo-controlled, parallel-group clinical trial was to examine the effects of electrical stimulation on cognition and behavior in AD patients who still live at home. Repeated measures analyses of variance revealed no effects of the intervention in the verum group (n = 32) compared with the placebo group (n = 30) on any of the cognitive and behavioral outcome measures. However, the majority of the patients and the caregivers evaluated the treatment procedure positively, and applying the daily treatment at home caused minimal burden. The lack of treatment effects calls for reconsideration of electrical stimulation as a symptomatic treatment in AD. [ABSTRACT FROM AUTHOR]
Published: 2005
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23. Can the Children's Communication Checklist differentiate between children with autism, children with ADHD, and normal controls?

Author: Geurts HM, Verté S, Oosterlaan J, Roeyers H, Hartman CA, Mulder EJ, van Berckelaer-Onnes IA, and Sergeant JA
Abstract: BACKGROUND: The Children's Communication Checklist (CCC; Bishop, 1998) is a questionnaire that was developed to measure pragmatic language use and may be completed by parents and teachers. Two studies are reported, which were designed to investigate: (1) whether children with Attention Deficit Hyperactivity Disorder (ADHD) encounter pragmatic language problems in comparison with normal controls (NC), (2) whether children with ADHD and children with High Functioning Autism (HFA) can be differentiated using the CCC, (3) the usefulness of the CCC for parents and teachers in a clinical and in a research setting, and (4) the role of age in pragmatic language use in ADHD and HFA. METHOD: In the first study (clinical sample) 50 children with ADHD, 50 children with HFA, and 50 NC were compared to each other using the CCC. In the second study (research sample) CCC data was gathered on 23 children with ADHD (without co-morbid disorders), 42 children with HFA, and 35 NC. RESULTS: Compared to NC, children with HFA showed pragmatic deficits on all CCC scales. Children with ADHD demonstrated deficits compared to NC as well. Moreover, the ADHD and HFA groups differed from each other on most of the scales. Discriminant analyses showed that CCC scales were relevant for case identification in these samples. Furthermore, profiles of impairment seen in children with HFA and ADHD did not vary with age. CONCLUSION: Pragmatic difficulties do occur in both HFA and ADHD. The present studies indicate that the CCC is a useful instrument to obtain information concerning pragmatic language use in both a clinical and a research setting. Although the information of parents is more tightly linked to the diagnosis, combining the information of both parent and teacher slightly improves case identification. [ABSTRACT FROM AUTHOR]
Published: 2004
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24. The Acute versus Chronic Pain Questionnaire (ACPQ) and actual pain experiences in older people.

Author: Scherder EJA, Smit R, Vuijk PJ, Bouma A, and Sergeant JA
Abstract: The Acute versus Chronic Pain Questionnaire (ACPQ) was applied to older people. Two groups emerged from an analysis of which an item of each pair (an acute and a chronic affective item) was considered to cause the most suffering. One group of subjects comprised those who expected to suffer more from one or more acute pain items (high-ACPQ group, n = 35). A second group emerged for whom none of the acute items was considered to be a burden (low-ACPQ group, n = 33). It was hypothesized that, compared to the low-ACPQ group, the subjects with high-ACPQ scores selected acute ACPQ-items due to a decline in the experience of chronic affective pain. This hypothesis predicted lower scores on the chronic ACPQ-items and lower scores on scales evaluating the subjects' own chronic affective pain. The results showed that, irrespective of the group, the chronic ACPQ-items were considered to produce the most burdens. However, compared with the low-ACPQ group, the high-ACPQ group reported experiencing significantly more pain from the acute ACPQ-items. Moreover, the latter group indicated suffering less pain from their own chronic pain conditions. The present findings suggest that the selection of one or more acute items of the ACPQ (high-ACPQ group) may point to an alteration in subjects' actual pain experience. [ABSTRACT FROM AUTHOR]
Published: 2002
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25. Seminar. Attention-deficit hyperactivity disorder and hyperkinetic disorder.

Author: Swanson JM, Sergeant JA, Taylor E, Sonuga-Barke EJS, Jensen PS, and Cantwell DP
Published: 1998
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26. LARGE-SCALE COMPLEXITY AND COGNITIVE CONTROL

Author: SERGEANT, JA, VLEK, CAJ, and Rijksuniversiteit Groningen
Published: 1983

27. Inhibitory performance, response speed, intraindividual variability, and response accuracy in ADHD.

Author: de Zeeuw P, Aarnoudse-Moens C, Bijlhout J, König C, Post Uiterweer A, Papanikolau A, Hoogenraad C, Imandt L, de Been D, Sergeant JA, and Oosterlaan J
Published: 2008
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28. Psychiatric genome-wide association study analyses implicate neuronal, immune and histone pathways

Author: Anita Thapar, Lena Backlund, Lindsey Kent, Walter J. Muir, A. Jeremy Willsey, Sandra K. Loo, Michael Boehnke, Christa Lese Martin, Ania Korszun, Guiomar Oliveira, Veronica J. Vieland, Stephen W. Scherer, René S. Kahn, Darina Czamara, Jeremy R. Parr, Michael E. Goddard, Willem A. Nolen, Josep Antoni Ramos-Quiroga, Stephen Sanders, Karola Rehnstroem, Nelson B. Freimer, Erin N. Smith, Ann Olincy, Ingrid Melle, Myrna M. Weissman, James A. Knowles, William Byerley, Aravinda Chakravarti, Shaun Purcell, Jens Treutlein, Sebastian Zoellner, Hakon Hakonarson, Susanne Lucae, Markus M. Noethen, Ian B. Hickie, Marion Friedl, Srinivasa Thirumalai, Stephen Newhouse, Joseph Piven, Andrew M. McIntosh, Cathryn M. Lewis, Srdjan Djurovic, Francis J. McMahon, Ayman H. Fanous, Bernie Devlin, Steven A. McCarroll, Alan F. Schatzberg, Peter Szatmari, Marta Ribasés, C. Robert Cloninger, Brenda W.J.H. Penninx, Gerard van Grootheest, Phil Lee, Richard Anney, Elaine K. Green, Geraldine Dawson, Joseph A. Sergeant, Digby Quested, Magdalena Gross, Jack D. Barchas, Nicholas G. Martin, Timothy W. Yu, Jouke-Jan Hottenga, Mark Lathrop, Federica Tozzi, Martin Hautzinger, Alysa E. Doyle, Cinnamon S. Bloss, Sandra Meier, Louise Gailagher, David A. Collier, Farooq Amin, Michael C. Neale, Martin Schalling, Lieuwe de Haan, Bru Cormand, Falk W. Lohoff, Jennifer Crosbie, Howard J. Edenberg, Aarno Palotie, Johannes H. Smit, Robert Freedman, Katherine Gordon-Smith, Michele L. Pergadia, Enda M. Byrne, Hans-Christoph Steinhausen, Benjamin M. Neale, Anjali K. Henders, Michele T. Pato, Manuel Mattheisen, Urban Ösby, Edward M. Scolnick, Evaristus A. Nwulia, Fritz Poustka, Gonneke Willemsen, Andrew C. Heath, David St. Cair, Emma M. Quinn, I. Nicol Ferrier, John R. Kelsoe, Vanessa Hus, Andrew McQuillin, John P. Rice, William M. McMahon, Joseph Biederman, Danyu Lin, Wolfgang Maier, Frans G. Zitman, Josephine Elia, Nicholas J. Schork, Stéphane Jamain, Lizzy Rossin, Jubao Duan, Ingrid Agartz, Devin Absher, Jordan W. Smoller, Matthew W. State, Richard M. Myers, Shrikant Mane, Carlos N. Pato, William E. Bunney, Marian L. Hamshere, Manfred Uhr, Nicholas John Craddock, Astrid M. Vicente, Tobias Banaschewski, David Curtis, Anne Farmer, Scott D. Gordon, Anna K. Kaehler, Eric M. Morrow, Marcella Rietschel, Patrik K. E. Magnusson, Klaus-Peter Lesch, Rebecca McKinney, Jana Strohmaier, Thomas F. Wienker, Pablo V. Gejman, Douglas Blackwood, Maria Helena Pinto de Azevedo, Tiffany A. Greenwood, Don H. Linszen, Daniel L. Koller, Richard Bruggeman, Vinay Puri, Naomi R. Wray, Stanley J. Watson, Elena Maestrini, Valentina Moskvina, Frank Dudbridge, Danielle Posthuma, Edward G. Jones, Lambertus Klei, Sarah E. Bergen, Fan Meng, Steven P. Hamilton, Guy A. Rouleau, Pierandrea Muglia, Mikael Landén, Stephanie H. Witt, Laramie E. Duncan, Stanley Zammit, Judith A. Badner, Florian Holsboer, Eco J. C. de Geus, Daniel Moreno-De-Luca, Benjamin S. Pickard, Gunnar Morken, Michael Conlon O'Donovan, Michael Steffens, Kathryn Roeder, Dorret I. Boomsma, Paul D. Shilling, Stephan Ripke, Nigel Williams, Jeremy M. Silverman, David Craig, Mark J. Daly, Michael Bauer, Detelina Grozeva, Markus J. Schwarz, Peter Holmans, Hugh Gurling, T. Scott Stroup, Aribert Rothenberger, Gary Donohoe, Eric Fombonne, Joseph D. Buxbaum, Matthew Flicldnger, Bryan J. Mowry, Thomas Hansen, Ina Giegling, Grant W. Montgomery, Caroline M. Nievergelt, Susan L. Smalley, Jung-Ying Tzeng, David H. Ledbetter, Christopher A. Walsh, Gerard D. Schellenberg, Sarah E. Medland, Robert D. Oades, James B. Potash, Dan E. Arking, Johannes Schumacher, Michael Gill, James J. McGough, Jennifer L. Moran, Donald W. Black, Sian Caesar, Neelroop N. Parikshak, Ian W. Craig, Sabine M. Klauck, Wade H. Berrettini, T. Foroud, Peter P. Zandi, Inez Myin-Germeys, Marcus Ising, Sven Cichon, Alexandre A. Todorov, Mònica Bayés, Thomas Werge, Susan L. Slager, Stanley I. Shyn, Jim van Os, Derek W. Morris, Douglas M. Ruderfer, Thomas W. Muehleisen, Matthew C. Keller, Susmita Datta, Ian Jones, John B. Vincent, James L. Kennedy, Anthony P. Monaco, Jianxin Shi, Dale R. Nyholt, Bruno Etain, Christine Fraser, Paul Cormican, Miguel Casas, Radhika Kandaswamy, Gerome Breen, Stephen V. Faraone, Jonna Kuntsi, Thomas Bettecken, Witte J.G. Hoogendijk, Nancy G. Buccola, Franziska Degenhardt, Lyudmila Georgieva, Marion Leboyer, Alan R. Sanders, John Strauss, Dan Rujescu, Russell Schachar, Helena Medeiros, Lisa Jones, Peter M. Visscher, Lauren A. Weiss, René Breuer, John I. Nurnberger, Andreas Reif, Phoenix Kwan, Vihra Milanova, Chunyu Liu, Martin A. Kohli, Donald J. MacIntyre, Nicholas Bass, Khalid Choudhury, Edwin H. Cook, Catherine Lord, Andrew D. Paterson, Jobst Meyer, Richard P. Ebstein, Zhaoming Zhao, Niklas Laengstroem, Thomas G. Schulze, Peter Propping, Wei Xu, Robert C. Thompson, Kimberly Chambert, Jonathan Pimm, Ivan Nikolov, Pamela A. F. Madden, Kevin A. McGhee, Jacob Lawrence, Jan K. Buitelaar, Andres Ingason, Christine M. Freitag, Robert Krasucki, Wiepke Cahn, Rita M. Cantor, Christina M. Hultman, Melvin G. McInnis, Catalina Betancur, Eftichia Duketis, Michael T. Murtha, Thomas H. Wassink, Philip Asherson, John S. Witte, Elaine Kenny, Edmund J.S. Sonuga-Barke, Lydia Krabbendam, Line Olsen, Agatino Battaglia, Laura J. Scott, Annette M. Hartmann, Yunjung Kim, Richard O. Day, Edwin J. C. G. van den Oord, Ole A. Andreassen, Herbert Roeyers, Michael John Owen, Colm O'Dushlaine, Peng Zhang, Morten Mattingsdal, Michael L. Cuccaro, Margaret A. Pericak-Vance, Joachim Hallmayer, Jun Li, Pamela B. Mahon, Elisabeth B. Binder, William A. Scheftner, Daniel H. Geschwind, Christel M. Middeldorp, Josef Frank, Keith Matthews, Jennifer K. Lowe, Paul Lichtenstein, Verneri Anttila, Pamela Sklar, Szabocls Szelinger, Roel A. Ophoff, Peter McGuffin, Stefan Herms, Bettina Konte, George Kirov, Hilary Coon, Maria Hipolito, Louise Frisén, Kenneth S. Kendler, Frank Bellivier, James S. Sutdiffe, Jeffrey A. Lieberman, Todd Lencz, Susanne Hoefels, Alan W. McLean, Barbara Franke, Huda Akil, Soumya Raychaudhuri, Ellen M. Wijsman, Vishwajit L. Nimgaonkar, Roy H. Perlis, Patrick J. McGrath, Susan L. Santangelo, William Coryell, Henrik B. Rasmussen, Weihua Guan, William Lawson, Elliot S. Gershon, Sean Ennis, Aiden Corvin, Allan H. Young, Thomas B. Barrett, Jonathan L. Haines, Douglas F. Levinson, Ana Miranda, Anil K. Malhotra, S. Hong Lee, Stan F. Nelson, Anthony J. Bailey, Patrick F. Sullivan, Dorothy E. Grice, Lefkos T. Middleton, Bertram Mueller-Myhsok, Michael R. Barnes, Adebayo Anjorin, O'Dushlaine, C, Rossin, L, Lee, Ph, Duncan, L, Parikshak, Nn, Newhouse, S, Ripke, S, Neale, Bm, Purcell, Sm, Posthuma, D, Nurnberger, Ji, Lee, Sh, Faraone, Sv, Perlis, Rh, Mowry, Bj, Thapar, A, Goddard, Me, Witte, J, Absher, D, Agartz, I, Akil, H, Amin, F, Andreassen, Oa, Anjorin, A, Anney, R, Anttila, V, Arking, De, Asherson, P, Azevedo, Mh, Backlund, L, Badner, Ja, Bailey, Aj, Banaschewski, T, Barchas, Jd, Barnes, Mr, Barrett, Tb, Bass, N, Battaglia, A, Bauer, M, Bayés, M, Bellivier, F, Bergen, Se, Berrettini, W, Betancur, C, Bettecken, T, Biederman, J, Binder, Eb, Black, Dw, Blackwood, Dh, Bloss, C, Boehnke, M, Boomsma, Di, Breuer, R, Bruggeman, R, Cormican, P, Buccola, Ng, Buitelaar, Jk, Bunney, We, Buxbaum, Jd, Byerley, Wf, Byrne, Em, Caesar, S, Cahn, W, Cantor, Rm, Casas, M, Chakravarti, A, Chambert, K, Choudhury, K, Cichon, S, Mattheisen, M, Cloninger, Cr, Collier, Da, Cook, Eh, Coon, H, Cormand, B, Corvin, A, Coryell, Wh, Craig, Dw, Craig, Iw, Crosbie, J, Cuccaro, Ml, Curtis, D, Czamara, D, Datta, S, Dawson, G, Day, R, De Geus, Ej, Degenhardt, F, Djurovic, S, Donohoe, Gj, Doyle, Ae, Duan, J, Dudbridge, F, Duketis, E, Ebstein, Rp, Edenberg, Hj, Elia, J, Ennis, S, Etain, B, Fanous, A, Farmer, Ae, Ferrier, In, Flickinger, M, Fombonne, E, Foroud, T, Frank, J, Franke, B, Fraser, C, Freedman, R, Freimer, Nb, Freitag, Cm, Friedl, M, Frisén, L, Gallagher, L, Gejman, Pv, Georgieva, L, Gershon, E, Giegling, I, Gill, M, Gordon, Sd, Gordon-Smith, K, Green, Ek, Greenwood, Ta, Grice, De, Gross, M, Grozeva, D, Guan, W, Gurling, H, De Haan, L, Haines, Jl, Hakonarson, H, Hallmayer, J, Hamilton, Sp, Hamshere, Ml, Hansen, Tf, Hartmann, Am, Hautzinger, M, Heath, Ac, Henders, Ak, Herms, S, Hickie, Ib, Hipolito, M, Hoefels, S, Holsboer, F, Hoogendijk, Wj, Hottenga, Jj, Hultman, Cm, Hus, V, Ingason, A, Ising, M, Jamain, S, Jones, Eg, Jones, I, Jones, L, Tzeng, Jy, Kähler, Ak, Kahn, R, Kandaswamy, R, Keller, Mc, Kennedy, Jl, Kenny, E, Kent, L, Kim, Y, Kirov, Gk, Klauck, Sm, Klei, L, Knowles, Ja, Kohli, Ma, Koller, Dl, Konte, B, Korszun, A, Krabbendam, L, Krasucki, R, Kuntsi, J, Kwan, P, Landén, M, Längström, N, Lathrop, M, Lawrence, J, Lawson, Wb, Leboyer, M, Ledbetter, Dh, Lencz, T, Lesch, Kp, Levinson, Df, Lewis, Cm, Li, J, Lichtenstein, P, Lieberman, Ja, Lin, Dy, Linszen, Dh, Liu, C, Lohoff, Fw, Loo, Sk, Lord, C, Lowe, Jk, Lucae, S, Macintyre, Dj, Madden, Pa, Maestrini, E, Magnusson, Pk, Mahon, Pb, Maier, W, Malhotra, Ak, Mane, Sm, Martin, Cl, Martin, Ng, Matthews, K, Mattingsdal, M, Mccarroll, Sa, Mcghee, Ka, Mcgough, Jj, Mcgrath, Pj, Mcguffin, P, Mcinnis, Mg, Mcintosh, A, Mckinney, R, Mclean, Aw, Mcmahon, Fj, Mcmahon, Wm, Mcquillin, A, Medeiros, H, Medland, Se, Meier, S, Melle, I, Meyer, J, Middeldorp, Cm, Middleton, L, Milanova, V, Miranda, A, Monaco, A, Montgomery, Gw, Moran, Jl, Moreno-De-Luca, D, Morken, G, Morris, Dw, Morrow, Em, Moskvina, V, Muglia, P, Mühleisen, Tw, Muir, Wj, Müller-Myhsok, B, Murtha, M, Myers, Rm, Myin-Germeys, I, Neale, Mc, Nelson, Sf, Nievergelt, Cm, Nikolov, I, Nimgaonkar, V, Nolen, Wa, Nöthen, Mm, Nwulia, Ea, Nyholt, Dr, Oades, Rd, Olincy, A, Oliveira, G, Olsen, L, Ophoff, Ra, Osby, U, Owen, Mj, Palotie, A, Parr, Jr, Paterson, Ad, Pato, Cn, Pato, Mt, Penninx, Bw, Pergadia, Ml, Pericak-Vance, Ma, Pickard, B, Pimm, J, Piven, J, Potash, Jb, Poustka, F, Propping, P, Puri, V, Quested, Dj, Quinn, Em, Ramos-Quiroga, Ja, Rasmussen, Hb, Raychaudhuri, S, Rehnström, K, Reif, A, Ribasés, M, Rice, Jp, Rietschel, M, Roeder, K, Roeyers, H, Rothenberger, A, Rouleau, G, Ruderfer, D, Rujescu, D, Sanders, Ar, Sanders, Sj, Santangelo, Sl, Sergeant, Ja, Schachar, R, Schalling, M, Schatzberg, Af, Scheftner, Wa, Schellenberg, Gd, Scherer, Sw, Schork, Nj, Schulze, Tg, Schumacher, J, Schwarz, M, Scolnick, E, Scott, Lj, Shi, J, Shilling, Pd, Shyn, Si, Silverman, Jm, Slager, Sl, Smalley, Sl, Smit, Jh, Smith, En, Sonuga-Barke, Ej, St Clair, D, State, M, Steffens, M, Steinhausen, Hc, Strauss, J, Strohmaier, J, Stroup, T, Sutcliffe, J, Szatmari, P, Szelinger, S, Thirumalai, S, Thompson, Rc, Todorov, Aa, Tozzi, F, Treutlein, J, Uhr, M, van den Oord, Jc, Van Grootheest, G, Van Os, J, Vicente, A, Vieland, Vj, Vincent, Jb, Visscher, Pm, Walsh, Ca, Wassink, Th, Watson, Sj, Weissman, Mm, Werge, T, Wienker, Tf, Wijsman, Em, Willemsen, G, Williams, N, Willsey, Aj, Witt, Sh, Xu, W, Young, Ah, Yu, Tw, Zammit, S, Zandi, Pp, Zhang, P, Zitman, Fg, Zöllner, S, Devlin, B, Kelsoe, Jr, Sklar, P, Daly, Mj, O'Donovan, Mc, Craddock, N, Kendler, K, Weiss, La, Wray, Nr, Zhao, Z, Geschwind, Dh, Sullivan, Pf, Smoller, Jw, Holmans, Pa, Breen, G., Génétique de l'autisme = Genetics of Autism (NPS-01), Neuroscience Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Human genetics, Psychiatry, NCA - Brain mechanisms in health and disease, NCA - Neurobiology of mental health, EMGO - Mental health, Child and Adolescent Psychiatry / Psychology, Epidemiology, Gastroenterology & Hepatology, Hematology, University of St Andrews. School of Medicine, University of St Andrews. Institute of Behavioural and Neural Sciences, Psychiatrie & Neuropsychologie, MUMC+: MA Psychiatrie (3), MUMC+: Hersen en Zenuw Centrum (3), RS: MHeNs - R2 - Mental Health, ANS - Amsterdam Neuroscience, Adult Psychiatry, Child Psychiatry, Universitat de Barcelona, Perceptual and Cognitive Neuroscience (PCN), Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Clinical Cognitive Neuropsychiatry Research Program (CCNP), Neurosciences Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Complex Trait Genetics, Biological Psychology, Educational Neuroscience, Clinical Neuropsychology, Neuroscience Campus Amsterdam - Brain Mechanisms in Health & Disease, LEARN! - Social cognition and learning, LEARN! - Brain, learning and development, Neuroscience Campus Amsterdam - Neurobiology of Mental Health, EMGO+ - Mental Health, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), O'Dushlaine, Colm, Rossin, Lizzy, Lee, Phil H, Duncan, Laramie, Lee, S Hong, Breen, Gerome, International Inflammatory Bowel Disease Genetics Consortium (IIBDGC), Network and Pathway Analysis Subgroup of the Psychiatric Genomics Consortium, and Myin-Germeys, Inez
Subjects: Netherlands Twin Register (NTR), Statistical methods, Autism, Medizin, LOCI, Genome-wide association study, heritability, Genome-wide association studies, Histones, Genètica mèdica, 0302 clinical medicine, Histone methylation, Databases, Genetic, 2.1 Biological and endogenous factors, Psychology, GWAS, Aetiology, Psychiatric genetics, R2C, bipolar disorder, Psychiatry, 0303 health sciences, Disorders, Loci, Depression, General Neuroscience, Mental Disorders, Medical genetics, METHYLATION, Brain, 3rd-DAS, Serious Mental Illness, Psychiatric Disorders, 3. Good health, Histone, Mental Health, Schizophrenia, Mental Disorder, Cognitive Sciences, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Promoters, BDC, BURDEN, RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry, Human, Signal Transduction, medicine.medical_specialty, DISORDERS, Genomics, Network and Pathway Analysis Subgroup of Psychiatric Genomics Consortium, Burden, Biology, Methylation, Article, Biological pathway, PROMOTERS, 03 medical and health sciences, Databases, Genetic, medicine, Genetics, Humans, Genetic Predisposition to Disease, histone methylation, Bipolar disorder, Psiquiatria, AUTISM, 030304 developmental biology, Genetic association, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Neurology & Neurosurgery, Neuroscience (all), Human Genome, Neurosciences, medicine.disease, Brain Disorders, Good Health and Well Being, DE-NOVO MUTATIONS, Perturbações do Desenvolvimento Infantil e Saúde Mental, RC0321, Genome-wide Association Studies, De-novo mutations, major depression, Neuroscience, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract: G.B. and S.N. acknowledge funding support for this work from the National Institute for Health Research (NIHR) Mental Health Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London. P.H.L. is supported by US National Institute of Mental Health (NIMH) grant K99MH101367. Genome-wide association studies (GWAS) of psychiatric disorders have identified multiple genetic associations with such disorders, but better methods are needed to derive the underlying biological mechanisms that these signals indicate. We sought to identify biological pathways in GWAS data from over 60,000 participants from the Psychiatric Genomics Consortium. We developed an analysis framework to rank pathways that requires only summary statistics. We combined this score across disorders to find common pathways across three adult psychiatric disorders: schizophrenia, major depression and bipolar disorder. Histone methylation processes showed the strongest association, and we also found statistically significant evidence for associations with multiple immune and neuronal signaling pathways and with the postsynaptic density. Our study indicates that risk variants for psychiatric disorders aggregate in particular biological pathways and that these pathways are frequently shared between disorders. Our results confirm known mechanisms and suggest several novel insights into the etiology of psychiatric disorders. Postprint
Published: 2015
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29. Differential distribution, affinity and plasticity of dopamine D-1 and D-2 receptors in the target sites of the mesolimbic system in an animal model of ADHD

Author: Felice J Esposito, Joseph A. Sergeant, Michele Papa, Linda M Diewald, Adolfo G. Sadile, Margaret P Carey, Mario Paolo Pellicano, Ugo Antonello Gironi Carnevale, Carey, Mp, Diewald, Lm, Esposito, Fj, Pellicano, Mp, GIRONI CARNEVALE, Ua, Sergeant, Ja, Papa, Michele, and Sadile, Adolfo
Subjects: Male, medicine.medical_specialty, Nucleus accumbens, Rats, Inbred WKY, Ventral pallidum, Behavioral Neuroscience, chemistry.chemical_compound, Mesencephalon, Rats, Inbred SHR, Internal medicine, Limbic System, medicine, Animals, Dopamine transporter, 7-OH-DPAT, Raclopride, Brain Mapping, Neuronal Plasticity, biology, Receptors, Dopamine D2, Receptors, Dopamine D1, Olfactory tubercle, Receptor Cross-Talk, Rats, Disease Models, Animal, Endocrinology, chemistry, Attention Deficit Disorder with Hyperactivity, Dopamine receptor, Islands of Calleja, biology.protein, Autoradiography, Neuroscience, medicine.drug
Abstract: The distribution of dopamine (DA) D-1 and D-2 receptors has been studied by autoradiography in the anterior forebrain of the pre-hypertensive spontaneously hypertensive rat (SHR) as an animal model of attention-deficit hyperactivity disorder (ADHD) in children. Juvenile male SHR and Wistar Kyoto (WKY) controls were given either vehicle or the DA re-uptake blocker methylphenidate (MP; 3 mg/kg, i.p.), daily during a 2-week period. A saturation analysis for the D-1 receptor subfamily was carried out with 0.1-5.0 nM of [3H]SCH23390 and two competition studies for the D-2 receptor subfamily with 4 nM of [3H]raclopride or 5 nM of [3H]quinpirole were carried out with unlabelled spiperone and 7-OH-DPAT as unlabelled displacers on cryostat coronal sections of the anterior forebrain. Quantitative receptor autoradiography and computer-assisted image analysis with reference to co-exposed 3H-microscale standards showed in vehicle-treated SHR higher density of DA D-1/D-5 receptor subtypes in the caudate-putamen (CPU), the nucleus accumbens (ACB) core and shell and the olfactory tubercle (OT), which was associated to a lower affinity. MP treatment normalised the DA D-1/D-5 receptors by decreasing the number of binding sites and increasing the affinity to control level. In addition, MP treatment 'down-regulated' DA D-2/D-4 subtypes in the CPU, ACB and OT, and 'up-regulated' mostly D-3 subtype in CPU, ACB, OT in both rat lines and in the globus pallidus, ventral pallidum and lateral septum in WKY rats only. In contrast, D-3 receptors were 'down-regulated' in the islands of Calleja in both rat lines. Moreover, regional cross-correlative analyses revealed a modulatory influence of DA receptors in the cross-talk within the anterior forebrain, which was altered in the SHR. Thus, the differential distribution and regulation of DA receptor subtypes following DA re-uptake blocker as well as the different regional cross-talk in the target sites of nigrostriatal and mesolimbic DA systems lend support to the DA hypothesis of ADHD in children.
Published: 1998
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30. Reduced transduction mechanisms in the anterior accumbal interface of an animal model of Attention-Deficit Hyperactivity Disorder

Author: Joseph A. Sergeant, Michele Papa, A.G. Sadile, Papa, Michele, Sergeant, Ja, and Sadile, Adolfo
Subjects: Male, medicine.medical_specialty, Central nervous system, Nucleus accumbens, Rats, Inbred WKY, Nucleus Accumbens, Behavioral Neuroscience, Spontaneously hypertensive rat, Species Specificity, Rats, Inbred SHR, Internal medicine, Ca2+/calmodulin-dependent protein kinase, Basal ganglia, medicine, Animals, Neurons, Basal forebrain, Chemistry, Ventral striatum, musculoskeletal system, Rats, medicine.anatomical_structure, Endocrinology, Microscopy, Fluorescence, Attention Deficit Disorder with Hyperactivity, Calcium-Calmodulin-Dependent Protein Kinases, cardiovascular system, Neuroscience, Immediate early gene, Signal Transduction, Transcription Factors
Abstract: The aim of this study was to map the neural substrates of attention-deficit hyperactivity disorder (ADHD) in the spontaneously hypertensive rat (SHR), which is thought to be a model for ADHD. To this aim, the Ca 2+ /calmodulin–dependent protein kinase II (CaMKII) and transcription factors (TF) were used as markers. The focus of interest was the nucleus accumbens complex (ACB) which is thought to be an interface between limbic and motor systems. Juvenile, male rats of the SHR line and Wistar–Kyoto (WKY) controls were perfused and the brains processed for immunocytochemistry for CaMKII and the TF peptides of the FOS , JUN-B and ZIF-268 families. The results revealed that: (i) in both groups there were more CaMKII-positive neurones in the shell than in the core of the ACB; (ii) SHR had a reduced number of CaMKII-positive elements in anterior portions of the shell; and (iii) SHR had a lower expression of peptide products of the FOS family ( c-FOS , in particular) and ZIF-268 . In addition, there was a lower expression of c-FOS and zif-268 in the core of the ACB in the SHR. In contrast, there was an increased basal level of JUN-B in the core of the ACB of SHR. The reduced number of CaMKII and TF-positive elements in the most rostral portions of the accumbal complex of SHR, associated to the higher number of binding sites for the DA D-1/D-5 subtype, appears as a discrete alteration in the prosomeric development of the anterior basal forebrain and could be the key to the understanding of ADHD.
Published: 1998
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31. Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs

Author: Laura J. Scott, Bernie Devlin, Steven A. McCarroll, James S. Sutcliffe, Stefan Herms, Yunjung Kim, Richard O. Day, Thomas F. Wienker, Frank Dudbridge, I. Nicol Ferrier, Bettina Konte, Marta Ribasés, C. Robert Cloninger, Brenda W.J.H. Penninx, Detelina Grozeva, Herbert Roeyers, Peter Holmans, Colm O'Dushlaine, Scott D. Gordon, Sarah E. Bergen, Fan Meng, Morten Mattingsdal, Hugh Gurling, Ina Giegling, Gerard van Grootheest, Ania Korszun, Markus J. Schwarz, George Kirov, Sebastian Zöllner, Kenneth S. Kendler, Nicholas G. Martin, Michael Conlon O'Donovan, Michael C. Neale, Jim van Os, Aravinda Chakravarti, Timothy W. Yu, Mikael Landén, Inez Myin-Germeys, Markus M. Nöthen, Kathryn Roeder, James B. Potash, Alan W. McLean, Louise Gallagher, Anna K. Kähler, Thomas Bettecken, Nigel Williams, Frank Bellivier, Joseph D. Buxbaum, Derek W. Morris, Susan L. Smalley, Jung-Ying Tzeng, Martin Schalling, Douglas M. Ruderfer, Caroline M. Nievergelt, T. Scott Stroup, David H. Ledbetter, Jennifer Crosbie, Anita Thapar, Barbara Franke, Jeffrey A. Lieberman, Huda Akil, Miguel Casas, Daniel H. Geschwind, Paul Cormican, Bertram Müller-Myhsok, Lyudmila Georgieva, Robert Krasucki, Martin Hautzinger, Alysa E. Doyle, Cinnamon S. Bloss, Gerard D. Schellenberg, Todd Lencz, Melvin G. McInnis, Catalina Betancur, Josep Antoni Ramos-Quiroga, Stephen Sanders, Eftichia Duketis, Don H. Linszen, Matthew W. State, Richard M. Myers, Soumya Raychaudhuri, Lizzy Rossin, Howard J. Edenberg, Michael E. Goddard, S. Hong Lee, Elisabeth B. Binder, Pablo V. Gejman, William A. Scheftner, Wolfgang Maier, Judith A. Badner, Christel M. Middeldorp, Maria Helena Pinto de Azevedo, Johannes H. Smit, Willem A. Nolen, Lieuwe de Haan, Gonneke Willemsen, Keith Matthews, Ellen M. Wijsman, Jennifer K. Lowe, Rebecca McKinney, Magdalena Gross, Dorothy E. Grice, James A. Knowles, Andrew C. Heath, Jana Strohmaier, Vishwajit L. Nimgaonkar, William Byerley, William E. Bunney, Dan E. Arking, Andrew McQuillin, William M. McMahon, Manuel Mattheisen, Hans-Christoph Steinhausen, Joseph Biederman, Guy A. Rouleau, James J. McGough, Sian Caesar, Edward M. Scolnick, Lefkos T. Middleton, Jack D. Barchas, Ian B. Hickie, Danyu Lin, Patrik K. E. Magnusson, Douglas Blackwood, Francis J. McMahon, Ingrid Agartz, Elena Maestrini, Marian L. Hamshere, Lindsey Kent, Walter J. Muir, Stephan Ripke, Lydia Krabbendam, Christine Fraser, Maria Hipolito, Louise Frisén, Eric Fombonne, Emma M. Quinn, Michael Bauer, Richard P. Ebstein, Michael Steffens, Jordan W. Smoller, Stanley J. Watson, Michael Boehnke, Philip Asherson, Agatino Battaglia, Elliot S. Gershon, Russell Schachar, Marcus Ising, Peng Zhang, Margaret A. Pericak-Vance, Joachim Hallmayer, Sean Ennis, Radhika Kandaswamy, René S. Kahn, Susanne Hoefels, Thomas W. Mühleisen, Pamela Sklar, Paul Lichtenstein, Verneri Anttila, Michael L. Cuccaro, Florian Holsboer, René Breuer, Eric M. Morrow, Vinay Puri, Naomi R. Wray, Szabocls Szelinger, Sabine M. Klauck, John B. Vincent, Shrikant Mane, Aribert Rothenberger, Marion Friedl, Ian Jones, Khalid Choudhury, Michael R. Barnes, Adebayo Anjorin, Edwin H. Cook, William Lawson, Allan H. Young, Lambertus Klei, Bryan J. Mowry, Johannes Schumacher, Michael Gill, James L. Kennedy, Marcella Rietschel, Aiden Corvin, Henrik B. Rasmussen, Susmita Datta, Kimberly Chambert, Daniel Moreno-De-Luca, Benjamin S. Pickard, Stan F. Nelson, Veronica J. Vieland, Stephen W. Scherer, Peter M. Visscher, John Strauss, Andreas Reif, Andrew D. Paterson, Ann Olincy, Phoenix Kwan, Anthony J. Bailey, Patrick F. Sullivan, Pierandrea Muglia, Gunnar Morken, Susanne Lucae, Ayman H. Fanous, Jacob Lawrence, Donald J. MacIntyre, Nancy G. Buccola, Rita M. Cantor, Christina M. Hultman, Weihua Guan, Anthony P. Monaco, Jouke-Jan Hottenga, Elaine Kenny, Jianxin Shi, Dale R. Nyholt, Kevin A. McGhee, Falk W. Lohoff, Jonna Kuntsi, Niklas Långström, John I. Nurnberger, Nelson B. Freimer, Erin N. Smith, John P. Rice, Michael T. Murtha, Thomas H. Wassink, Alexandre A. Todorov, Edmund J.S. Sonuga-Barke, Dan Rujescu, Roy H. Perlis, John S. Witte, Christopher A. Walsh, Matthew C. Keller, Pamela B. Mahon, Patrick J. McGrath, Susan L. Santangelo, Annette M. Hartmann, Ole A. Andreassen, Tatiana Foroud, Shaun Purcell, Josef Frank, Douglas F. Levinson, William Coryell, Ana Miranda, Alan F. Schatzberg, Peter Szatmari, Jun Li, Gerome Breen, Stephen V. Faraone, Anil K. Malhotra, Helena Medeiros, Martin A. Kohli, Nicholas Bass, Catherine Lord, Peter Propping, Wei Xu, Federica Tozzi, Ivan Nikolov, Jan K. Buitelaar, Thomas G. Schulze, Katherine Gordon-Smith, Michele L. Pergadia, Fritz Poustka, Valentina Moskvina, David Curtis, Tobias Banaschewski, Devin Absher, Danielle Posthuma, Stanley Zammit, Gary Donohoe, Ingrid Melle, Karola Rehnström, Thomas Hansen, Myrna M. Weissman, Stanley I. Shyn, Hakon Hakonarson, Christa Lese Martin, Digby Quested, Darina Czamara, Jeremy R. Parr, Pamela A. F. Madden, Jens Treutlein, Aarno Palotie, Robert Freedman, Sandra Meier, Bru Cormand, Nicholas J. Schork, Michele T. Pato, John R. Kelsoe, Vanessa Hus, Frans G. Zitman, Josephine Elia, David St Clair, Roel A. Ophoff, Peter McGuffin, Jonathan Pimm, Jonathan L. Haines, Wiepke Cahn, Matthew Flickinger, Steven P. Hamilton, Michael John Owen, Paul D. Shilling, Jeremy M. Silverman, David Craig, Mark J. Daly, Sarah E. Medland, Robert D. Oades, Marion Leboyer, Alan R. Sanders, Vihra Milanova, Chunyu Liu, Jobst Meyer, Dorret I. Boomsma, Evaristus A. Nwulia, Thomas B. Barrett, Jennifer L. Moran, Donald W. Black, Mònica Bayés, Witte J.G. Hoogendijk, Franziska Degenhardt, Benjamin M. Neale, Daniel L. Koller, Carlos N. Pato, Nicholas John Craddock, Richard Bruggeman, Enda M. Byrne, Edward G. Jones, Eco J. C. de Geus, Stéphane Jamain, Jubao Duan, Anne Farmer, Astrid M. Vicente, Grant W. Montgomery, Thomas Werge, Cathryn M. Lewis, Srdjan Djurovic, Phil Lee, Richard Anney, Elaine K. Green, Wade H. Berrettini, Peter P. Zandi, Susan L. Slager, Stephanie H. Witt, Ian W. Craig, Lisa Jones, Sven Cichon, Bruno Etain, Mark Lathrop, Hilary Coon, Robert C. Thompson, Lena Backlund, A. Jeremy Willsey, Andres Ingason, Christine M. Freitag, Sandra K. Loo, Guiomar Oliveira, Line Olsen, Edwin J. C. G. van den Oord, Geraldine Dawson, Joseph A. Sergeant, David A. Collier, Farooq Amin, Srinivasa Thirumalai, Manfred Uhr, Joseph Piven, Andrew M. McIntosh, Anjali K. Henders, Urban Ösby, Klaus-Peter Lesch, Tiffany A. Greenwood, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Perceptual and Cognitive Neuroscience (PCN), Lee, S Hong, Ripke, Stephan, Neale, Benjamin M, Faraone, Stephen V, Wray, Naomi R, Cross-Disorder Group of the Psychiatric Genomics Consortium, International Inflammatory Bowel Disease Genetics Consortium (IIBDGC), Queensland Brain Institute, University of Queensland [Brisbane], Massachusetts General Hospital [Boston], Harvard Medical School [Boston] (HMS), Broad Institute of MIT and Harvard (BROAD INSTITUTE), Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston], SUNY Upstate Medical University, State University of New York (SUNY), Mount Sinai School of Medicine, Department of Psychiatry-Icahn School of Medicine at Mount Sinai [New York] (MSSM), Psychiatric and Neurodevelopmental Genetics Unit, Queensland Centre for Mental Health Research, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University, MRC Centre for Neuropsychiatric Genetics and Genomics, Medical Research Council (MRC)-School of Medicine [Cardiff], Cardiff University-Institute of Medical Genetics [Cardiff]-Cardiff University-Institute of Medical Genetics [Cardiff], New South Wales Department of Primary Industries (NSW DPI), Faculty of Land and Food Resources, University of Melbourne, HudsonAlpha Institute for Biotechnology [Huntsville, AL], Institute of Clinical Medicine [Oslo], Faculty of Medicine [Oslo], University of Oslo (UiO)-University of Oslo (UiO), Diakonhjemmet Hospital, University of Michigan [Ann Arbor], University of Michigan System, Molecular and Behavioral Neuroscience Institute (MBNI), University of Michigan System-University of Michigan System, Emory University [Atlanta, GA], Oslo University Hospital [Oslo], University College of London [London] (UCL), Trinity College Dublin, Johns Hopkins University School of Medicine [Baltimore], MRC Social Genetic Developmental and Psychiatry Centre, Institute of Psychiatry, King's College London, University of Coimbra [Portugal] (UC), Karolinska Institutet [Stockholm], University of Chicago, University of British Columbia (UBC), Department of Child and Adolescent Psychiatry and Psychotherapy [Mannheim], Universität Heidelberg [Heidelberg] = Heidelberg University, Weill Medical College of Cornell University [New York], GlaxoSmithKline, Glaxo Smith Kline, Portland Veterans Administration Medical Center, Windeyer Institute for Medical Sciences, IRCCS Fondazione Stella Maris [Pisa], University Hospital Carl Gustav Carus [Dresden, Germany], Technische Universität Dresden = Dresden University of Technology (TU Dresden), Centro Nacional de Analisis Genomico [Barcelona] (CNAG), Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Diderot - Paris 7 (UPD7), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), European Network of Bipolar Research Expert Centres (ENBREC), ENBREC, Department of Psychiatry [Philadelphia], University of Pennsylvania, Physiopathologie des Maladies du Système Nerveux Central, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Unité de recherche Phytopharmacie et Médiateurs Chimiques (UPMC), Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Max Planck Institute of Psychiatry, Max-Planck-Gesellschaft, Massachusetts General Hospital [Boston, MA, USA], University of Iowa [Iowa City], University of Edinburgh, Royal Hospital for Sick Children [Edinburgh], The Scripps Research Institute [La Jolla, San Diego], MRC Social, Genetic and Developmental Psychiatry Centre (SGDP), King‘s College London-The Institute of Psychiatry, Institute of Medical Sciences, University of Aberdeen, Social, Genetic and Developmental Psychiatry Centre (SGDP), King‘s College London, Department of Genetic Epidemiology in Psychiatry [Mannhein], Universität Heidelberg [Heidelberg] = Heidelberg University-Central Institute of Mental Health Mannheim, Department of Psychiatry, University of Groningen [Groningen]-University Medical Center Groningen [Groningen] (UMCG), Trinity College Dublin-St. James's Hospital, School of Nursing, Louisiana State University (LSU), Donders Center for Cognitive Neuroimaging, Donders Centre for Cognitive Neuroimaging, Radboud University [Nijmegen]-Radboud University [Nijmegen], Department of Psychiatry and Human Behavior, University of California [Irvine] (UC Irvine), University of California (UC)-University of California (UC), Friedman Brain Institute, Mount Sinai, Icahn School of Medicine at Mount Sinai [New York] (MSSM), Seaver Autism Center for Research and Treatment, Department of Neuroscience, Departments of Psychiatry, Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai [New York] (MSSM)-Seaver Autism Center-, The Mindich Child Health & Development Institute, Friedman Brain Institute, The Mindich Child Health and Development Institute, University of California [San Francisco] (UC San Francisco), Department of Psychiatry, School of Clinical and Experimental Medicine, University of Alabama at Birmingham [ Birmingham] (UAB), Department of Human Genetics, Los Angeles, David Geffen School of Medicine [Los Angeles], University of California [Los Angeles] (UCLA), University of California (UC)-University of California (UC)-University of California [Los Angeles] (UCLA), McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Stanley Center for Psychiatric Research, Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston]-Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston], Mental Health Sciences Unit, Department of Genomics, Life and Brain Center, Universität Bonn = University of Bonn, Institute of Human Genetics, Institute of Neuroscience and Medicine (INM-1), Research Center Juelich, Academic Department of Child and Adolescent Psychiatry, Institute of Psychiatry, Department of Disability and Human Development, University of Illinois [Chicago] (UIC), University of Illinois System-University of Illinois System, Department of Developmental Neuroscience, Neuropsychiatric Genetics Research Group, University of California [San Diego] (UC San Diego), John P. Hussman Institute for Human Genomics, University of Miami [Coral Gables], East London NHS Foundation Trust, Queen Mary University of London (QMUL), Max-Planck-Institut für Psychiatrie, Genetics Institute, Autism Speaks and the Department of Psychiatry, University of North Carolina [Chapel Hill] (UNC), University of North Carolina System (UNC)-University of North Carolina System (UNC), School of Neurology, Neurobiology and Psychiatry, Royal Victoria Infirmary, Medstar Research Institute, KG Jebsen Centre for Psychosis Research, University of Oslo (UiO)-Institute of Clinical Medicine-Oslo University Hospital [Oslo], Deparment of Medical Genetics, Human Genetics Branch, National Institutes of Health [Bethesda] (NIH)-National Institute of Mental Health (NIMH), Harvard Medical School [Boston] (HMS)-Massachusetts General Hospital [Boston], Department of Psychiatry and Behavioral Sciences, University of Chicago-NorthShore University Health System, Department of Non-Communicable Disease Epidemiology, London School of Hygiene and Tropical Medicine (LSHTM), Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, Goethe-Universität Frankfurt am Main, Psychology Department, National University of Singapore (NUS), Department of Biochemistry and Molecular Biology, Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indiana University System-Indiana University System, Academic Centre on Rare Diseases (ACoRD), University College Dublin [Dublin] (UCD), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Service de psychiatrie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Hôpital Albert Chenevier, Virginia Institute of Psychiatric and Behavioral Genetics, Virginia Commonwealth University (VCU), University of Dundee School of Medicine, University of Dundee, Department of Biostatistics and Center for Statistical Genetics, University of Michigan System-University of Michigan System-School of public health, The University of Hong Kong (HKU)-The University of Hong Kong (HKU), Department of Child Psychiatry, McGill University = Université McGill [Montréal, Canada]-Montreal Children's Hospital, McGill University Health Center [Montreal] (MUHC)-McGill University Health Center [Montreal] (MUHC), Howard University College of Medicine, University of Colorado [Denver], Center for Neurobehavioral Genetics, Department of Genomics, Department of Molecular Medicine, Department of Neurology, University of California (UC)-University of California (UC)-David Geffen School of Medicine [Los Angeles], Medical Research Council-Cardiff University, Department of Psychiatry [Pittsburgh], University of Pittsburgh School of Medicine, Pennsylvania Commonwealth System of Higher Education (PCSHE)-Pennsylvania Commonwealth System of Higher Education (PCSHE), Fisico-Quimica Biologica, Universidade Federal do Rio de Janeiro (UFRJ), Vanderbilt Brain Institute, Vanderbilt University School of Medicine [Nashville], Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania-University of Pennsylvania-Children’s Hospital of Philadelphia (CHOP ), The Center for Applied Genomics, Children’s Hospital of Philadelphia (CHOP ), Stanford School of Medicine [Stanford], Stanford Medicine, Stanford University-Stanford University, Institute for Human Genetics, Neurosciences Centre of Excellence in Drug Discovery, GlaxoSmithKline Research and Development, Center for Genomic Medicine, Copenhagen University Hospital-Rigshospitalet [Copenhagen], Copenhagen University Hospital, Department of Clinical and Developmental Psychology, Eberhard Karls Universität Tübingen = Eberhard Karls University of Tuebingen, Clinical Research Unit, Brain & Mind Research Institute-The University of Sydney, Functional Genomics, Neuronal Plasticity / Mouse Behaviour, Erasmus University Medical Center [Rotterdam] (Erasmus MC), Department of Medical Epidemiology and Biostatistics (MEB), Autism and Communicative Disorders Centre, Center for Human Genetic Research, Center for neuroscience-University of California [Davis] (UC Davis), Bioinformatics Research Center, North Carolina State University [Raleigh] (NC State), Norwegian University of Science and Technology [Trondheim] (NTNU), Norwegian University of Science and Technology (NTNU)-Norwegian University of Science and Technology (NTNU), Emory University [Atlanta, GA]-Atlanta Veterans Affairs Medical Center, Psychiatric Neurogenetics Section, Centre for Addiction and Mental Health, School of Medicine, University of St Andrews [Scotland], Institute of Human Genetics [Erlangen, Allemagne], Friedrich-Alexander Universität Erlangen-Nürnberg (FAU), Division of Molecular Genome Analysis, German Cancer Research Center - Deutsches Krebsforschungszentrum [Heidelberg] (DKFZ), Department of Ecology and Evolutionary Biology, Insitute of Neuroscience and Physiology, University of Gothenburg (GU), Institut de Génomique d'Evry (IG), Université Paris-Saclay-Institut de Biologie François JACOB (JACOB), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Developmental Brain and Behaviour Unit, University of Southampton, Division of Psychiatric Genomics, Rheinische Friedrich-Wilhelms-Universität Bonn, Statistical Genetics Group, Department of Human Genetics, Department of Pharmacy and Biotechnology, Alma Mater Studiorum Università di Bologna [Bologna] (UNIBO), Department of Psychiatry and Psychotherapy, Department of Mental Health, Johns Hopkins University and Hospital, W.M. Keck Biotechnology Resource Laboratory, Yale University [New Haven], Institutes of Neuroscience and Health and Society, Newcastle University [Newcastle], Genetic Epidemiology Unit, Queensland Institute of Medical Research, Department of Biomedicine and the Centre for Integrative Sequencing, Aarhus University [Aarhus], Sorlandet Hospital HF, Division of Psychiatry, University of Edinburgh-Royal Edinburgh Hospital, Medical Genetics Section, University of Edinburgh-Western General Hospital, Unit on the Genetic Basis of Mood and Anxiety Disorders, National Institutes of Health [Bethesda] (NIH), Unidade de Neurodesenvolvimento e Autismo (UNDA), Hospital Pediatrico de Coimbra, Division of Mental Health and Addiction, Molecular Psychiatry Laboratory, University of Michigan System-University of Michigan System-Molecular and Behavioral Neuroscience Institute, Research and Development, First Psychiatric Clinic-Alexander University Hospital, Registo Oncológico Regional-Sul, Instituto Português de Oncologia de Francisco Gentil, The Wellcome Trust Centre for Human Genetics [Oxford], University of Oxford, St. Olav's Hospital, Brown University, Department of Molecular Biology, Cell Biology and Biochemistry, Translational Centre for Regenerative Medicine (TRM), Department of Cell Therapy, Universität Leipzig-Universität Leipzig, Human Genetics Department, University of Pittsburgh (PITT), Institute for Biomedical Imaging and Life Science, University Medical Center [Utrecht]-Brain Center Rudolf Magnus, Head of Medical Sequencing, Program in Genetics and Genomic Biology, Hospital for Sick Children-University of Toronto McLaughlin Centre, The Centre for Applied Genomics, Toronto, The Hospital for sick children [Toronto] (SickKids)-University of Toronto-Department of Molecular Genetics-McLaughlin Centre, Carolina Institute for Developmental Disabilities, Analytic and Translational Genetics Unit, Rush University Medical Center [Chicago], Julius-Maximilians-Universität Würzburg (JMU), Washington University in Saint Louis (WUSTL), Department of Statistics, Carnegie Mellon University [Pittsburgh] (CMU), Department of Experimental Clinical and Health Psychology, Universiteit Gent = Ghent University (UGENT), Department of Child and Adolescent Psychiatry, Georg-August-University = Georg-August-Universität Göttingen, Department of Medicine, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CR CHUM), Centre Hospitalier de l'Université de Montréal (CHUM), Université de Montréal (UdeM)-Université de Montréal (UdeM)-Centre Hospitalier de l'Université de Montréal (CHUM), Université de Montréal (UdeM)-Université de Montréal (UdeM), Departments of Psychiatry and Genetics, Yale School of Medicine [New Haven, Connecticut] (YSM), Maine Medical Center, Free University of Amsterdam, Department of Psychiatry and Behavioral Sciences [Stanford], Pathology and Laboratory Medicine, The Scripps Translational Science Institute and The Scripps Research Institute, Psychiatric Center Nordbaden, Division of Cancer Epidemiology and Genetics, National Cancer Institute [Bethesda] (NCI-NIH), National Institutes of Health [Bethesda] (NIH)-National Institutes of Health [Bethesda] (NIH), The Scripps Translational Science Institute and Scripps Health, Child and Adolescent Psychiatry, Aarhus University Hospital, Molecular Neuropsychiatry and Development Laboratory, Department of Molecular Physiology & Biophysics and Psychiatry, Vanderbilt University [Nashville]-Centers for Human Genetics Research and Molecular Neuroscience, Department of Psychiatry and Behavioural Neurosciences, McMaster University [Hamilton, Ontario]-Offord Centre for Child Studies, The Translational Genomics Research Institute (TGen), Oxford Health NHS Foundation Trust, Marlborough House Secure Unit, Instituto Nacional de Saùde Dr Ricardo Jorge [Portugal] (INSA), BioFIG, Center for Biodiversity, Functional and Integrative Genomics, Battelle Center for Mathematical Medicine, Ohio State University [Columbus] (OSU)-Nationwide Children's Hospital, University of Toronto, Diamantina Institute, Carver College of Medicine [Iowa City], University of Iowa [Iowa City]-University of Iowa [Iowa City], Departments of Biostatistics and Medicine, University of Washington [Seattle], ArcelorMittal Maizières Research SA, ArcelorMittal, Institute of Mental Health, Johns Hopkins Bloomberg School of Public Health [Baltimore], Johns Hopkins University (JHU)-Johns Hopkins University (JHU), Psychiatrie & Neuropsychologie, Farmacologie en Toxicologie, RS: CARIM School for Cardiovascular Diseases, RS: MHeNs School for Mental Health and Neuroscience, Biological Psychology, Educational Neuroscience, Clinical Neuropsychology, Neuroscience Campus Amsterdam - Brain Mechanisms in Health & Disease, LEARN! - Social cognition and learning, Biophotonics and Medical Imaging, Neuroscience Campus Amsterdam - Neurobiology of Mental Health, LEARN! - Brain, learning and development, EMGO+ - Mental Health, LEARN!, Neuroscience Campus Amsterdam - Brain Imaging Technology, LaserLaB - Biophotonics and Microscopy, State University of New York (SUNY)-State University of New York (SUNY), Department of Neuroscience and Physiology, Faculty of Land and Environment, Biosciences Research Division, Department of Environment and Primary Industries Victoria, Department of Epidemiology and Biostatistics, University of California [San Francisco] (UCSF), University of California-University of California, Universität Heidelberg [Heidelberg], Cornell University [New York]-Weill Medical College of Cornell University [New York], Bioinformatics, Internal Medicine, Portland Va Medical Center : Ganzini Linda MD, Technische Universität Dresden = Dresden University of Technology (TU Dresden)-University Hospital Carl Gustav Carus, Centro Nacional de Análisis Genómico (CNAG), Parc Científic de Barcelona (PCB), University of Pennsylvania [Philadelphia], Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), Clinical and Research Programs in Pediatric Psychopharmacology and Adult ADHD, Division Genetic Epidemiology in Psychiatry, Central Institute of Mental Health [Mannheim], Medical Faculty [Mannheim]-Medical Faculty [Mannheim], Universität Heidelberg [Heidelberg]-Central Institute of Mental Health Mannheim, Radboud university [Nijmegen]-Radboud university [Nijmegen], University of California [Irvine] (UCI), University of California-University of California-University of California [Los Angeles] (UCLA), University of Bonn, University of California-University of California-David Geffen School of Medicine [Los Angeles], Cardiff University-Medical Research Council, University of Pennsylvania [Philadelphia]-University of Pennsylvania [Philadelphia]-Children’s Hospital of Philadelphia (CHOP ), Bureau d'Économie Théorique et Appliquée (BETA), Institut National de la Recherche Agronomique (INRA)-Université de Strasbourg (UNISTRA)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Institut de Biologie François JACOB (JACOB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, University of Oxford [Oxford], Universität Leipzig [Leipzig]-Universität Leipzig [Leipzig], University of Toronto-The Hospital for sick children [Toronto] (SickKids)-Department of Molecular Genetics-McLaughlin Centre, Julius-Maximilians-Universität Würzburg [Wurtzbourg, Allemagne] (JMU), Universiteit Gent = Ghent University [Belgium] (UGENT), University of Göttingen - Georg-August-Universität Göttingen, Yale University School of Medicine, Georg-August-University [Göttingen], ANS - Amsterdam Neuroscience, Adult Psychiatry, Child Psychiatry, Psychiatry, Human genetics, NCA - Brain mechanisms in health and disease, NCA - Neurobiology of mental health, EMGO - Mental health, NCA - Brain imaging technology, Lee SH, Ripke S, Neale BM, Faraone SV, Purcell SM, Perlis RH, Mowry BJ, Thapar A, Goddard ME, Witte JS, Absher D, Agartz I, Akil H, Amin F, Andreassen OA, Anjorin A, Anney R, Anttila V, Arking DE, Asherson P, Azevedo MH, Backlund L, Badner JA, Bailey AJ, Banaschewski T, Barchas JD, Barnes MR, Barrett TB, Bass N, Battaglia A, Bauer M, Bayés M, Bellivier F, Bergen SE, Berrettini W, Betancur C, Bettecken T, Biederman J, Binder EB, Black DW, Blackwood DH, Bloss CS, Boehnke M, Boomsma DI, Breen G, Breuer R, Bruggeman R, Cormican P, Buccola NG, Buitelaar JK, Bunney WE, Buxbaum JD, Byerley WF, Byrne EM, Caesar S, Cahn W, Cantor RM, Casas M, Chakravarti A, Chambert K, Choudhury K, Cichon S, Cloninger CR, Collier DA, Cook EH, Coon H, Cormand B, Corvin A, Coryell WH, Craig DW, Craig IW, Crosbie J, Cuccaro ML, Curtis D, Czamara D, Datta S, Dawson G, Day R, De Geus EJ, Degenhardt F, Djurovic S, Donohoe GJ, Doyle AE, Duan J, Dudbridge F, Duketis E, Ebstein RP, Edenberg HJ, Elia J, Ennis S, Etain B, Fanous A, Farmer AE, Ferrier IN, Flickinger M, Fombonne E, Foroud T, Frank J, Franke B, Fraser C, Freedman R, Freimer NB, Freitag CM, Friedl M, Frisén L, Gallagher L, Gejman PV, Georgieva L, Gershon ES, Geschwind DH, Giegling I, Gill M, Gordon SD, Gordon-Smith K, Green EK, Greenwood TA, Grice DE, Gross M, Grozeva D, Guan W, Gurling H, De Haan L, Haines JL, Hakonarson H, Hallmayer J, Hamilton SP, Hamshere ML, Hansen TF, Hartmann AM, Hautzinger M, Heath AC, Henders AK, Herms S, Hickie IB, Hipolito M, Hoefels S, Holmans PA, Holsboer F, Hoogendijk WJ, Hottenga JJ, Hultman CM, Hus V, Ingason A, Ising M, Jamain S, Jones EG, Jones I, Jones L, Tzeng JY, Kähler AK, Kahn RS, Kandaswamy R, Keller MC, Kennedy JL, Kenny E, Kent L, Kim Y, Kirov GK, Klauck SM, Klei L, Knowles JA, Kohli MA, Koller DL, Konte B, Korszun A, Krabbendam L, Krasucki R, Kuntsi J, Kwan P, Landén M, Långström N, Lathrop M, Lawrence J, Lawson WB, Leboyer M, Ledbetter DH, Lee PH, Lencz T, Lesch KP, Levinson DF, Lewis CM, Li J, Lichtenstein P, Lieberman JA, Lin DY, Linszen DH, Liu C, Lohoff FW, Loo SK, Lord C, Lowe JK, Lucae S, MacIntyre DJ, Madden PA, Maestrini E, Magnusson PK, Mahon PB, Maier W, Malhotra AK, Mane SM, Martin CL, Martin NG, Mattheisen M, Matthews K, Mattingsdal M, McCarroll SA, McGhee KA, McGough JJ, McGrath PJ, McGuffin P, McInnis MG, McIntosh A, McKinney R, McLean AW, McMahon FJ, McMahon WM, McQuillin A, Medeiros H, Medland SE, Meier S, Melle I, Meng F, Meyer J, Middeldorp CM, Middleton L, Milanova V, Miranda A, Monaco AP, Montgomery GW, Moran JL, Moreno-De-Luca D, Morken G, Morris DW, Morrow EM, Moskvina V, Muglia P, Mühleisen TW, Muir WJ, Müller-Myhsok B, Murtha M, Myers RM, Myin-Germeys I, Neale MC, Nelson SF, Nievergelt CM, Nikolov I, Nimgaonkar V, Nolen WA, Nöthen MM, Nurnberger JI, Nwulia EA, Nyholt DR, O'Dushlaine C, Oades RD, Olincy A, Oliveira G, Olsen L, Ophoff RA, Osby U, Owen MJ, Palotie A, Parr JR, Paterson AD, Pato CN, Pato MT, Penninx BW, Pergadia ML, Pericak-Vance MA, Pickard BS, Pimm J, Piven J, Posthuma D, Potash JB, Poustka F, Propping P, Puri V, Quested DJ, Quinn EM, Ramos-Quiroga JA, Rasmussen HB, Raychaudhuri S, Rehnström K, Reif A, Ribasés M, Rice JP, Rietschel M, Roeder K, Roeyers H, Rossin L, Rothenberger A, Rouleau G, Ruderfer D, Rujescu D, Sanders AR, Sanders SJ, Santangelo SL, Sergeant JA, Schachar R, Schalling M, Schatzberg AF, Scheftner WA, Schellenberg GD, Scherer SW, Schork NJ, Schulze TG, Schumacher J, Schwarz M, Scolnick E, Scott LJ, Shi J, Shilling PD, Shyn SI, Silverman JM, Slager SL, Smalley SL, Smit JH, Smith EN, Sonuga-Barke EJ, St Clair D, State M, Steffens M, Steinhausen HC, Strauss JS, Strohmaier J, Stroup TS, Sutcliffe JS, Szatmari P, Szelinger S, Thirumalai S, Thompson RC, Todorov AA, Tozzi F, Treutlein J, Uhr M, van den Oord EJ, Van Grootheest G, Van Os J, Vicente AM, Vieland VJ, Vincent JB, Visscher PM, Walsh CA, Wassink TH, Watson SJ, Weissman MM, Werge T, Wienker TF, Wijsman EM, Willemsen G, Williams N, Willsey AJ, Witt SH, Xu W, Young AH, Yu TW, Zammit S, Zandi PP, Zhang P, Zitman FG, Zöllner S, Devlin B, Kelsoe JR, Sklar P, Daly MJ, O'Donovan MC, Craddock N, Sullivan PF, Smoller JW, Kendler KS, Wray NR, Cardiff University-Medical Research Council (MRC), HudsonAlpha Institute for Biotechnology, The Institute of Psychiatry-King‘s College London, Cornell University-Weill Medical College of Cornell University [New York], Stanford University Medical School, Technische Universität Dresden (TUD)-University Hospital Carl Gustav Carus, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-Hôpital Albert Chenevier, McGill University-Montreal Children's Hospital, Universidade Federal do Rio de Janeiro [Rio de Janeiro] (UFRJ), Stanford University School of Medicine [Stanford], Stanford University [Stanford], Eberhard Karls Universität Tübingen, Friedrich Alexander University [Erlangen-Nürnberg], Università di Bologna [Bologna] (UNIBO), University of Toronto-The Hospital for Sick Children-Department of Molecular Genetics-McLaughlin Centre, Washington University School of Medicine, Ghent University [Belgium] (UGENT), University of Goettingen, CHUM Research Center, Psychiatry and Behavioral Science, Stanford University School of Medicine [CA, USA], Aalborg Psychiatric Hospital, Aarhus University Hospital, Washington University in St Louis, Instituto Nacional de Saude Dr Ricardo Jorge, Oades, Robert D., Guellaen, Georges, Medical Oncology, Epidemiology, Child and Adolescent Psychiatry / Psychology, and Hematology
Subjects: Netherlands Twin Register (NTR), Medizin, Inheritance Patterns, Social Sciences, AUTISM SPECTRUM DISORDERS, nosology, heritability, COMMON SNPS, 0302 clinical medicine, Crohn Disease, SCHIZOPHRENIA, Child, Psychiatric genetics, Genetics & Heredity, MAJOR DEPRESSIVE DISORDER, RISK, 0303 health sciences, ATTENTION-DEFICIT/HYPERACTIVITY DISORDER, 120 000 Neuronal Coherence, Mental Disorders, Variants, BIPOLAR DISORDER, ASSOCIATION, Genomic disorders and inherited multi-system disorders [DCN PAC - Perception action and control IGMD 3], Psychiatric Disorders, CROHNS-DISEASE, 3. Good health, Schizophrenia, genetic association study, Medical genetics, Major depressive disorder, SNPs, Adult, medicine.medical_specialty, genetic etiology, medical genetics, DEFICIT HYPERACTIVITY DISORDER, Biology, Polymorphism, Single Nucleotide, behavioral disciplines and activities, Article, Genomic disorders and inherited multi-system disorders DCN MP - Plasticity and memory [IGMD 3], Heritability, Genetic Heterogeneity, 03 medical and health sciences, Prevalence of mental disorders, mental disorders, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Genetics, medicine, ddc:61, Humans, Attention deficit hyperactivity disorder, Genetic Predisposition to Disease, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, DCN PAC - Perception action and control NCEBP 9 - Mental health, ddc:610, Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie, Psychosomatik und Psychotherapie des Kindes- und Jugendalters, Bipolar disorder, Psychiatry, 030304 developmental biology, Depressive Disorder, Major, Genome, Human, Genetic heterogeneity, medicine.disease, schizophrenia, Attention Deficit Disorder with Hyperactivity, Child Development Disorders, Pervasive, Perturbações do Desenvolvimento Infantil e Saúde Mental, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract: AM Vicente - Cross-Disorder Group of the Psychiatric Genomics Consortium Most psychiatric disorders are moderately to highly heritable. The degree to which genetic variation is unique to individual disorders or shared across disorders is unclear. To examine shared genetic etiology, we use genome-wide genotype data from the Psychiatric Genomics Consortium (PGC) for cases and controls in schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD). We apply univariate and bivariate methods for the estimation of genetic variation within and covariation between disorders. SNPs explained 17-29% of the variance in liability. The genetic correlation calculated using common SNPs was high between schizophrenia and bipolar disorder (0.68 ± 0.04 s.e.), moderate between schizophrenia and major depressive disorder (0.43 ± 0.06 s.e.), bipolar disorder and major depressive disorder (0.47 ± 0.06 s.e.), and ADHD and major depressive disorder (0.32 ± 0.07 s.e.), low between schizophrenia and ASD (0.16 ± 0.06 s.e.) and non-significant for other pairs of disorders as well as between psychiatric disorders and the negative control of Crohn's disease. This empirical evidence of shared genetic etiology for psychiatric disorders can inform nosology and encourages the investigation of common pathophysiologies for related disorders.
Published: 2013
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32. NMDA and non-NMDA sensitive [l-3H] glutamate receptor binding in the brain of the Naples high- and low-excitability rats: an autoradiographic study

Author: Joseph A. Sergeant, Terje Sagvolden, A.G. Sadile, Mario P. Pellicano, Onderzoeksinstituut Psychologie (FMG), Sadile, Adolfo, Pellicano, Mp, Sagvolden, T, and Sergeant, Ja
Subjects: Male, medicine.medical_specialty, N-Methylaspartate, Hippocampus, AMPA receptor, Motor Activity, Hippocampal formation, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, Glutamate receptor binding, Behavioral Neuroscience, Species Specificity, Internal medicine, Genetic model, Excitatory Amino Acid Agonists, medicine, Animals, Receptor, Brain Chemistry, Chemistry, Glutamate receptor, Brain, Quisqualic Acid, Rats, Endocrinology, Receptors, Glutamate, nervous system, Attention Deficit Disorder with Hyperactivity, Autoradiography, NMDA receptor
Abstract: The Naples high-excitability (NHE) and low-excitability (NLE) rat lines, selectively bred for high and low activity in a Làt maze, respectively, are used as an animal model in the study of hippocampal functions. The aim of this study was to investigate the anatomical distribution of N-methyl-d-aspartate (NMDA) and non-NMDA sensitive [3H]glutamate receptor binding by quantitative autoradiography in the brain of the NHE and NLE rats with a randomly bred line (NRB) as controls. Twenty-micron-thick cryostat sagittal sections were incubated at 4°C with 150 nM [l-3H]glutamate alone or in the presence of 100 μM NMDA or 2.5 μM quisqualate (QA). Non-specific binding was determined in the presence of 1 mM of non-labeled glutamate. The sections were exposed to tritium-sensitive films for 3 weeks at 4°C. Quantitative analysis revealed: (1) higher levels of total binding in NHE than in NRB and NLE rats in all areas but the cerebellum; (2) fewer binding sites for both NMDA and QA receptors and larger binding sites for QA receptors in the hippocampus of NLE and NHE rats, respectively; (3) a positive correlation between total binding sites and activity level in a Làt maze in all areas, except the cerebellar molecular layer with NLE < NHE, which was due to a differential contribution from NMDA and non-NMDA types. Thus, the brain of the NHE rats shows an imbalance between NMDA and non-NMDA sensitive [l-3H]glutamate receptors.
Published: 1996
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33. Aspects of ADHD in Adults: Neurocognitive functioning, actigraphy, effects of methylphenidate, and association with genetic polymorphsims

Author: Boonstra, AM, Buitelaar, JK, Sergeant, JA, Oosterlaan, J, and Department of Psychology, Education and Child Studies
Published: 2006

34. Non-selective attention and nitric oxide in putative animal models of Attention-Deficit Hyperactivity Disorder

Author: Joseph A. Sergeant, A.G. Sadile, Ugo Antonello Gironi Carnevale, Raffaele Aspide, Aspide, R, GIRONI CARNEVALE, Ua, Sergeant, Ja, and Sadile, Adolfo
Subjects: Male, medicine.medical_specialty, media_common.quotation_subject, Nitric Oxide, Rats, Inbred WKY, Nitric oxide, Behavioral Neuroscience, chemistry.chemical_compound, Spontaneously hypertensive rat, Internal medicine, Rats, Inbred SHR, medicine, Attention deficit hyperactivity disorder, Animals, Learning, Attention, Selective attention, Enzyme Inhibitors, media_common, biology, business.industry, Single injection, medicine.disease, Rats, Nitric oxide synthase, Endocrinology, NG-Nitroarginine Methyl Ester, chemistry, Enzyme inhibitor, Attention Deficit Disorder with Hyperactivity, biology.protein, Nitric Oxide Synthase, business, Neuroscience, Vigilance (psychology)
Abstract: Non-selective attention (NSA) to environmental stimuli has been measured in putative animal models of Attention-Deficit Hyperactivity Disorder (ADHD), such as the Spontaneously Hypertensive (SHR) and the Naples High-Excitability (NHE) rat lines. A series of experiments has been carried out on male juvenile SHR and Wistar-Kyoto (WKY) controls (experiment 1) and on the NHE and two controls, i.e. the Naples Low-Excitability (NLE) and a random-bred (NRB) line (experiment 2). It was done under basal conditions or following a single injection of the nitric oxide synthase (NOS) inhibitor L-nitro-arginine-methylester (L-NAME: 0.1-10 mg/kg, i.p.), or vehicle, 30 min before testing on day 1 and vehicle alone before testing on days 2 and 3 in SHR/WKY (experiment 3) and the Naples lines (experiment 4). The behavior in a Lat maze during three consecutive 10-min exposures at 24-h intervals was monitored by a CCD video camera and analyzed off-line for frequency and duration of rearings on hindlimbs per 1-min blocks. The results demonstrated that both SHR and NHE rats showed a higher frequency of rearings of shorter duration than controls. With time of testing, the duration of rearings tended to increase in the WKY but not the SHR. In the Naples lines the duration tended to increase in all but mostly in the NHE rats. The acute inhibition of NOS by L-NAME significantly increased the duration of rearing episodes both in SHR and NHE rats only at 10 mg/kg in the second part of the testing period. Therefore, NSA, as indexed by the duration of rearings, is defective in both hyperactivity models against different genetic backgrounds. In addition, this impairment is dependent upon nitric oxide (NO), which appears to play a significant role in these processes.
Published: 1998

35. Reduced CaMKII-positive neurones in the accumbens shell of an animal model of Attention-Deficit Hyperactivity disorder

Author: Joseph A. Sergeant, Terje Sagvolden, Adolfo G. Sadile, Michele Papa, Onderzoeksinstituut Psychologie (FMG), Papa, M, Sagvolden, T, Sergeant, Ja, and Sadile, Adolfo
Subjects: Male, Central nervous system, Nucleus accumbens, Rats, Inbred WKY, Nucleus Accumbens, Spontaneously hypertensive rat, Animal model, Ca2+/calmodulin-dependent protein kinase, Rats, Inbred SHR, Motor system, Basal ganglia, medicine, Attention deficit hyperactivity disorder, Animals, Attention, cardiovascular diseases, Neurons, General Neuroscience, musculoskeletal system, medicine.disease, Immunohistochemistry, Rats, Isoenzymes, medicine.anatomical_structure, Attention Deficit Disorder with Hyperactivity, Calcium-Calmodulin-Dependent Protein Kinases, cardiovascular system, Psychology, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Neuroscience
Abstract: THIS study aimed at investigating putative neural substrates of attention-deficit hyperactivity disorder in children using the spontaneously hypertensive rat (SHR) as animal model and the Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) as a marker in the nucleus accumbens, an interface between limbic and motor systems. In prehypertensive male SHR and Wistar-Kyoto rats image analysis of CaMKII immunocyto-chemistry showed more positive elements in the shell than in the core, and in the former a lower level in SHR. The data indicate a reduced number of nucleus accumbens modules available for limbic-motor integration revealing putative substrates of the altered attentional and reinforcement mechanisms demonstrated in the SHR and in children with attention-deficit hyperactivity disorder.
Published: 1996

36. Differential expression of transcription factors in the accumbens of an animal model of ADHD

Author: Joseph A. Sergeant, Michele Papa, Adolfo G. Sadile, Papa, Michele, Sergeant, Ja, Sadile, Adolfo, and Onderzoeksinstituut Psychologie (FMG)
Subjects: Male, Neural substrate, General Neuroscience, Immunocytochemistry, Central nervous system, Gene Expression, Nucleus accumbens, Rats, Inbred WKY, Nucleus Accumbens, Rats, Immunoenzyme Techniques, Basal (phylogenetics), medicine.anatomical_structure, Attention Deficit Disorder with Hyperactivity, Rats, Inbred SHR, Basal ganglia, medicine, Animals, Psychology, Genes, Immediate-Early, Neuroscience, Immediate early gene, Transcription factor, Transcription Factors
Abstract: Transcription factors have been used as neuronal markers in the nucleus accumbens (ACB) of male juvenile spontaneously hypertensive rats (SHR), an animal model of attention-deficit hyperactivity disorder (ADHD), to trace putative neural substrates. In SHR, immunocytochemistry and PC-assisted image analysis showed lower expression of pan-fos, c-fos, zif/268 in the shell, and the c-fos and zif/268 in the core, with an increased level of Jun-B in the core. The differential lower basal expression of transcription factors in the ACB of an animal model of ADHD implies a reduced number of modules and might represent a neural substrate of the attention deficits seen in SHR and children with ADHD at low motivational levels.

37. The influence of Generalized Anxiety Disorder on Executive Functions in children with ADHD.

Author: Menghini D, Armando M, Calcagni M, Napolitano C, Pasqualetti P, Sergeant JA, Pani P, and Vicari S
Subjects: Adolescent, Anxiety Disorders epidemiology, Attention Deficit Disorder with Hyperactivity epidemiology, Child, Female, Humans, Inhibition, Psychological, Male, Neuropsychological Tests, Psychiatric Status Rating Scales, Statistics, Nonparametric, Anxiety Disorders complications, Attention Deficit Disorder with Hyperactivity complications, Executive Function physiology
Abstract: The present study was aimed at verifying whether the presence of generalized anxiety disorder (GAD) affects executive functions in children with attention-deficit hyperactivity disorder (ADHD). Two groups of children with ADHD were selected for the study according to the presence or absence of GAD. The first group of 28 children with ADHD with GAD (mean age: 9 ± 1.2; males/females: 24/4) was matched for gender, age, IQ, psychiatric comorbidity with a second group of 29 children with ADHD without GAD (mean age: 8.8 ± 0.7; males/females: 26/3). The two groups with ADHD were compared to 28 typically developing children (mean age: 8.3 ± 1.3; males/females: 23/5) on different measures involving processes especially important in inhibitory control such as rule maintenance, stimulus detection, action selection and action execution. Our results indicated that, differently from children with ADHD with GAD, only the group with ADHD without GAD showed a deficit in inhibitory control. Comorbid subgroups should be differentiated, especially, to develop specific and efficient therapeutic interventions in ADHD.
Published: 2018
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38. Familiality of Co-existing ADHD and Tic Disorders: Evidence from a Large Sibling Study.

Author: Roessner V, Banaschewski T, Becker A, Buse J, Wanderer S, Buitelaar JK, Sergeant JA, Sonuga-Barke EJ, Gill M, Manor I, Miranda A, Mulas F, Oades RD, Roeyers H, Steinhausen HC, Faraone SV, Asherson P, and Rothenberger A
Abstract: Background: The association of attention-deficit/hyperactivity disorder (ADHD) and tic disorder (TD) is frequent and clinically important. Very few and inconclusive attempts have been made to clarify if and how the combination of ADHD+TD runs in families., Aim: To determine the first time in a large-scale ADHD sample whether ADHD+TD increases the risk of ADHD+TD in siblings and, also the first time, if this is independent of their psychopathological vulnerability in general., Methods: The study is based on the International Multicenter ADHD Genetics (IMAGE) study. The present sub-sample of 2815 individuals included ADHD-index patients with co-existing TD (ADHD+TD, n = 262) and without TD (ADHD-TD, n = 947) as well as their 1606 full siblings (n = 358 of the ADHD+TD index patients and n = 1248 of the ADHD-TD index patients). We assessed psychopathological symptoms in index patients and siblings by using the Strength and Difficulties Questionnaire (SDQ) and the parent and teacher Conners' long version Rating Scales (CRS). For disorder classification the Parental Account of Childhood Symptoms (PACS-Interview) was applied in n = 271 children. Odds ratio with the GENMOD procedure (PROCGENMOD) was used to test if the risk for ADHD, TD, and ADHD+TD in siblings was associated with the related index patients' diagnoses. In order to get an estimate for specificity we compared the four groups for general psychopathological symptoms., Results: Co-existing ADHD+TD in index patients increased the risk of both comorbid ADHD+TD and TD in the siblings of these index patients. These effects did not extend to general psychopathology., Interpretation: Co-existence of ADHD+TD may segregate in families. The same holds true for TD (without ADHD). Hence, the segregation of TD (included in both groups) seems to be the determining factor, independent of further behavioral problems. This close relationship between ADHD and TD supports the clinical approach to carefully assess ADHD in any case of TD.
Published: 2016
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39. Angiogenic, neurotrophic, and inflammatory system SNPs moderate the association between birth weight and ADHD symptom severity.

Author: Smith TF, Anastopoulos AD, Garrett ME, Arias-Vasquez A, Franke B, Oades RD, Sonuga-Barke E, Asherson P, Gill M, Buitelaar JK, Sergeant JA, Kollins SH, Faraone SV, and Ashley-Koch A
Subjects: Angiogenesis Inducing Agents therapeutic use, Attention Deficit Disorder with Hyperactivity drug therapy, Birth Weight, Female, Humans, Inflammation genetics, Male, Parents, Attention Deficit Disorder with Hyperactivity genetics, Nerve Growth Factors genetics, Polymorphism, Single Nucleotide genetics
Abstract: Low birth weight is associated with increased risk for Attention-Deficit/Hyperactivity Disorder (ADHD); however, the etiological underpinnings of this relationship remain unclear. This study investigated if genetic variants in angiogenic, dopaminergic, neurotrophic, kynurenine, and cytokine-related biological pathways moderate the relationship between birth weight and ADHD symptom severity. A total of 398 youth from two multi-site, family-based studies of ADHD were included in the analysis. The sample consisted of 360 ADHD probands, 21 affected siblings, and 17 unaffected siblings. A set of 164 SNPs from 31 candidate genes, representing five biological pathways, were included in our analyses. Birth weight and gestational age data were collected from a state birth registry, medical records, and parent report. Generalized Estimating Equations tested for main effects and interactions between individual SNPs and birth weight centile in predicting ADHD symptom severity. SNPs within neurotrophic (NTRK3) and cytokine genes (CNTFR) were associated with ADHD inattentive symptom severity. There was no main effect of birth weight centile on ADHD symptom severity. SNPs within angiogenic (NRP1 & NRP2), neurotrophic (NTRK1 & NTRK3), cytokine (IL16 & S100B), and kynurenine (CCBL1 & CCBL2) genes moderate the association between birth weight centile and ADHD symptom severity. The SNP main effects and SNP × birth weight centile interactions remained significant after adjusting for multiple testing. Genetic variability in angiogenic, neurotrophic, and inflammatory systems may moderate the association between restricted prenatal growth, a proxy for an adverse prenatal environment, and risk to develop ADHD., (© 2014 Wiley Periodicals, Inc.)
Published: 2014
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40. Quantitative linkage for autism spectrum disorders symptoms in attention-deficit/hyperactivity disorder: significant locus on chromosome 7q11.

Author: Nijmeijer JS, Arias-Vásquez A, Rommelse NN, Altink ME, Buschgens CJ, Fliers EA, Franke B, Minderaa RB, Sergeant JA, Buitelaar JK, Hoekstra PJ, and Hartman CA
Subjects: Attention, Child, Child Development Disorders, Pervasive physiopathology, Chromosome Mapping, Female, Humans, Male, Surveys and Questionnaires, Attention Deficit Disorder with Hyperactivity genetics, Child Development Disorders, Pervasive genetics, Chromosomes, Human, Pair 7 genetics, Genetic Linkage
Abstract: We studied 261 ADHD probands and 354 of their siblings to assess quantitative trait loci associated with autism spectrum disorder symptoms (as measured by the Children's Social Behavior Questionnaire (CSBQ)) using a genome-wide linkage approach, followed by locus-wide association analysis. A genome-wide significant locus for the CSBQ subscale addressing social interaction was found on chromosome 7q11, with suggestive signals supporting this locus on three other CSBQ subscales. We identified two other suggestive loci for the CSBQ total scale and individual subscales on chromosomes 4q35 and 7p12. Fine-mapping the significantly linked locus resulted in interesting candidate genes, although their association was not significant after permutation testing.
Published: 2014
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41. Authors' reply.

Author: Groenman AP, Oosterlaan J, Rommelse NN, Franke B, Greven CU, Hoekstra PJ, Hartman CA, Luman M, Roeyers H, Oades RD, Sergeant JA, Buitelaar JK, and Faraone SV
Subjects: Female, Humans, Male, Attention Deficit Disorder with Hyperactivity drug therapy, Attention Deficit and Disruptive Behavior Disorders drug therapy, Central Nervous System Stimulants adverse effects, Conduct Disorder drug therapy, Substance-Related Disorders etiology, Tobacco Use Disorder etiology
Published: 2014
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42. Abnormal striatal BOLD responses to reward anticipation and reward delivery in ADHD.

Author: Furukawa E, Bado P, Tripp G, Mattos P, Wickens JR, Bramati IE, Alsop B, Ferreira FM, Lima D, Tovar-Moll F, Sergeant JA, and Moll J
Subjects: Adult, Case-Control Studies, Female, Humans, Magnetic Resonance Imaging, Male, Young Adult, Attention Deficit Disorder with Hyperactivity physiopathology, Corpus Striatum physiology, Reward
Abstract: Altered reward processing has been proposed to contribute to the symptoms of attention deficit hyperactivity disorder (ADHD). The neurobiological mechanism underlying this alteration remains unclear. We hypothesize that the transfer of dopamine release from reward to reward-predicting cues, as normally observed in animal studies, may be deficient in ADHD. Functional magnetic resonance imaging (fMRI) was used to investigate striatal responses to reward-predicting cues and reward delivery in a classical conditioning paradigm. Data from 14 high-functioning and stimulant-naïve young adults with elevated lifetime symptoms of ADHD (8 males, 6 females) and 15 well-matched controls (8 males, 7 females) were included in the analyses. During reward anticipation, increased blood-oxygen-level-dependent (BOLD) responses in the right ventral and left dorsal striatum were observed in controls, but not in the ADHD group. The opposite pattern was observed in response to reward delivery; the ADHD group demonstrated significantly greater BOLD responses in the ventral striatum bilaterally and the left dorsal striatum relative to controls. In the ADHD group, the number of current hyperactivity/impulsivity symptoms was inversely related to ventral striatal responses during reward anticipation and positively associated with responses to reward. The BOLD response patterns observed in the striatum are consistent with impaired predictive dopamine signaling in ADHD, which may explain altered reward-contingent behaviors and symptoms of ADHD.
Published: 2014
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43. Candidate genetic pathways for attention-deficit/hyperactivity disorder (ADHD) show association to hyperactive/impulsive symptoms in children with ADHD.

Author: Bralten J, Franke B, Waldman I, Rommelse N, Hartman C, Asherson P, Banaschewski T, Ebstein RP, Gill M, Miranda A, Oades RD, Roeyers H, Rothenberger A, Sergeant JA, Oosterlaan J, Sonuga-Barke E, Steinhausen HC, Faraone SV, Buitelaar JK, and Arias-Vásquez A
Subjects: Adolescent, Attention Deficit Disorder with Hyperactivity epidemiology, Child, Child, Preschool, Europe epidemiology, Female, Genotype, Humans, Hyperkinesis epidemiology, Impulsive Behavior epidemiology, Israel epidemiology, Male, Phenotype, Psychiatric Status Rating Scales, Severity of Illness Index, Attention Deficit Disorder with Hyperactivity genetics, Genetic Association Studies methods, Hyperkinesis genetics, Impulsive Behavior genetics
Abstract: Objective: Because multiple genes with small effect sizes are assumed to play a role in attention-deficit/hyperactivity disorder (ADHD) etiology, considering multiple variants within the same analysis likely increases the total explained phenotypic variance, thereby boosting the power of genetic studies. This study investigated whether pathway-based analysis could bring scientists closer to unraveling the biology of ADHD., Method: The pathway was described as a predefined gene selection based on a well-established database or literature data. Common genetic variants in pathways involved in dopamine/norepinephrine and serotonin neurotransmission and genes involved in neuritic outgrowth were investigated in cases from the International Multicentre ADHD Genetics (IMAGE) study. Multivariable analysis was performed to combine the effects of single genetic variants within the pathway genes. Phenotypes were DSM-IV symptom counts for inattention and hyperactivity/impulsivity (n = 871) and symptom severity measured with the Conners Parent (n = 930) and Teacher (n = 916) Rating Scales., Results: Summing genetic effects of common genetic variants within the pathways showed a significant association with hyperactive/impulsive symptoms ((p)empirical = .007) but not with inattentive symptoms ((p)empirical = .73). Analysis of parent-rated Conners hyperactive/impulsive symptom scores validated this result ((p)empirical = .0018). Teacher-rated Conners scores were not associated. Post hoc analyses showed a significant contribution of all pathways to the hyperactive/impulsive symptom domain (dopamine/norepinephrine, (p)empirical = .0004; serotonin, (p)empirical = .0149; neuritic outgrowth, (p)empirical = .0452)., Conclusion: The present analysis shows an association between common variants in 3 genetic pathways and the hyperactive/impulsive component of ADHD. This study demonstrates that pathway-based association analyses, using quantitative measurements of ADHD symptom domains, can increase the power of genetic analyses to identify biological risk factors involved in this disorder., (Copyright © 2013 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.)
Published: 2013
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44. Proactive and reactive control of movement are differently affected in Attention Deficit Hyperactivity Disorder children.

Author: Pani P, Menghini D, Napolitano C, Calcagni M, Armando M, Sergeant JA, and Vicari S
Subjects: Child, Child Behavior, Female, Humans, Individuality, Male, Neuropsychological Tests, Reaction Time physiology, Attention Deficit Disorder with Hyperactivity physiopathology, Attention Deficit Disorder with Hyperactivity psychology, Inhibition, Psychological, Movement physiology, Psychomotor Performance physiology
Abstract: Attention-Deficit/Hyperactivity Disorder children are impaired in the ability to interrupt an ongoing action in relation to a sudden change in the environment (reactive control, measured by stop signal reaction time, SSRT). Less investigated is the ability to control the response when it is known in advance that it will be required to stop (proactive control, measured by change in Reaction time, RT). The study is aimed at exploring both the reactive and the proactive inhibitory control in a group of ADHD children compared to a group of age-matched controls. ADHD children (N=28) and Controls (N=28) performed 4 tasks: 2 tasks required to respond to the appearance of the go-signals (go task and nostop task) and 2 tasks to respond to the go signals in a context in which sometimes a restrain or suppression of the response was required (go-nogo task and stop task). ADHD children showed a longer SSRT compared to controls. Both groups showed an increment in RT by comparing the go-nogo to the go task and an increment in RT and SD by comparing the stop to the nostop task. ADHD children showed higher intra-individual variability (SD) compared to controls only in the stop and nostop task. ADHD children showed impaired reactive control but preserved proactive control, and the physical appearance of the go signal affected their reaction times intra-individual variability. A comparison between the reactive and proactive controls helps in defining neuropsychological profiles of ADHD children and can inspires therapeutic behavioral-cognitive strategies for response control., (Copyright © 2013 Elsevier Ltd. All rights reserved.)
Published: 2013
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45. Association between DRD2/DRD4 interaction and conduct disorder: a potential developmental pathway to alcohol dependence.

Author: Mota NR, Bau CH, Banaschewski T, Buitelaar JK, Ebstein RP, Franke B, Gill M, Kuntsi J, Manor I, Miranda A, Mulas F, Oades RD, Roeyers H, Rothenberger A, Sergeant JA, Sonuga-Barke EJ, Steinhausen HC, Faraone SV, and Asherson P
Subjects: Adolescent, Child, Comorbidity, Conduct Disorder complications, Female, Humans, Male, Prognosis, Alcoholism etiology, Conduct Disorder genetics, Polymorphism, Genetic genetics, Receptors, Dopamine D2 genetics, Receptors, Dopamine D4 genetics
Published: 2013
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46. Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs.

Author: Lee SH, Ripke S, Neale BM, Faraone SV, Purcell SM, Perlis RH, Mowry BJ, Thapar A, Goddard ME, Witte JS, Absher D, Agartz I, Akil H, Amin F, Andreassen OA, Anjorin A, Anney R, Anttila V, Arking DE, Asherson P, Azevedo MH, Backlund L, Badner JA, Bailey AJ, Banaschewski T, Barchas JD, Barnes MR, Barrett TB, Bass N, Battaglia A, Bauer M, Bayés M, Bellivier F, Bergen SE, Berrettini W, Betancur C, Bettecken T, Biederman J, Binder EB, Black DW, Blackwood DH, Bloss CS, Boehnke M, Boomsma DI, Breen G, Breuer R, Bruggeman R, Cormican P, Buccola NG, Buitelaar JK, Bunney WE, Buxbaum JD, Byerley WF, Byrne EM, Caesar S, Cahn W, Cantor RM, Casas M, Chakravarti A, Chambert K, Choudhury K, Cichon S, Cloninger CR, Collier DA, Cook EH, Coon H, Cormand B, Corvin A, Coryell WH, Craig DW, Craig IW, Crosbie J, Cuccaro ML, Curtis D, Czamara D, Datta S, Dawson G, Day R, De Geus EJ, Degenhardt F, Djurovic S, Donohoe GJ, Doyle AE, Duan J, Dudbridge F, Duketis E, Ebstein RP, Edenberg HJ, Elia J, Ennis S, Etain B, Fanous A, Farmer AE, Ferrier IN, Flickinger M, Fombonne E, Foroud T, Frank J, Franke B, Fraser C, Freedman R, Freimer NB, Freitag CM, Friedl M, Frisén L, Gallagher L, Gejman PV, Georgieva L, Gershon ES, Geschwind DH, Giegling I, Gill M, Gordon SD, Gordon-Smith K, Green EK, Greenwood TA, Grice DE, Gross M, Grozeva D, Guan W, Gurling H, De Haan L, Haines JL, Hakonarson H, Hallmayer J, Hamilton SP, Hamshere ML, Hansen TF, Hartmann AM, Hautzinger M, Heath AC, Henders AK, Herms S, Hickie IB, Hipolito M, Hoefels S, Holmans PA, Holsboer F, Hoogendijk WJ, Hottenga JJ, Hultman CM, Hus V, Ingason A, Ising M, Jamain S, Jones EG, Jones I, Jones L, Tzeng JY, Kähler AK, Kahn RS, Kandaswamy R, Keller MC, Kennedy JL, Kenny E, Kent L, Kim Y, Kirov GK, Klauck SM, Klei L, Knowles JA, Kohli MA, Koller DL, Konte B, Korszun A, Krabbendam L, Krasucki R, Kuntsi J, Kwan P, Landén M, Långström N, Lathrop M, Lawrence J, Lawson WB, Leboyer M, Ledbetter DH, Lee PH, Lencz T, Lesch KP, Levinson DF, Lewis CM, Li J, Lichtenstein P, Lieberman JA, Lin DY, Linszen DH, Liu C, Lohoff FW, Loo SK, Lord C, Lowe JK, Lucae S, MacIntyre DJ, Madden PA, Maestrini E, Magnusson PK, Mahon PB, Maier W, Malhotra AK, Mane SM, Martin CL, Martin NG, Mattheisen M, Matthews K, Mattingsdal M, McCarroll SA, McGhee KA, McGough JJ, McGrath PJ, McGuffin P, McInnis MG, McIntosh A, McKinney R, McLean AW, McMahon FJ, McMahon WM, McQuillin A, Medeiros H, Medland SE, Meier S, Melle I, Meng F, Meyer J, Middeldorp CM, Middleton L, Milanova V, Miranda A, Monaco AP, Montgomery GW, Moran JL, Moreno-De-Luca D, Morken G, Morris DW, Morrow EM, Moskvina V, Muglia P, Mühleisen TW, Muir WJ, Müller-Myhsok B, Murtha M, Myers RM, Myin-Germeys I, Neale MC, Nelson SF, Nievergelt CM, Nikolov I, Nimgaonkar V, Nolen WA, Nöthen MM, Nurnberger JI, Nwulia EA, Nyholt DR, O'Dushlaine C, Oades RD, Olincy A, Oliveira G, Olsen L, Ophoff RA, Osby U, Owen MJ, Palotie A, Parr JR, Paterson AD, Pato CN, Pato MT, Penninx BW, Pergadia ML, Pericak-Vance MA, Pickard BS, Pimm J, Piven J, Posthuma D, Potash JB, Poustka F, Propping P, Puri V, Quested DJ, Quinn EM, Ramos-Quiroga JA, Rasmussen HB, Raychaudhuri S, Rehnström K, Reif A, Ribasés M, Rice JP, Rietschel M, Roeder K, Roeyers H, Rossin L, Rothenberger A, Rouleau G, Ruderfer D, Rujescu D, Sanders AR, Sanders SJ, Santangelo SL, Sergeant JA, Schachar R, Schalling M, Schatzberg AF, Scheftner WA, Schellenberg GD, Scherer SW, Schork NJ, Schulze TG, Schumacher J, Schwarz M, Scolnick E, Scott LJ, Shi J, Shilling PD, Shyn SI, Silverman JM, Slager SL, Smalley SL, Smit JH, Smith EN, Sonuga-Barke EJ, St Clair D, State M, Steffens M, Steinhausen HC, Strauss JS, Strohmaier J, Stroup TS, Sutcliffe JS, Szatmari P, Szelinger S, Thirumalai S, Thompson RC, Todorov AA, Tozzi F, Treutlein J, Uhr M, van den Oord EJ, Van Grootheest G, Van Os J, Vicente AM, Vieland VJ, Vincent JB, Visscher PM, Walsh CA, Wassink TH, Watson SJ, Weissman MM, Werge T, Wienker TF, Wijsman EM, Willemsen G, Williams N, Willsey AJ, Witt SH, Xu W, Young AH, Yu TW, Zammit S, Zandi PP, Zhang P, Zitman FG, Zöllner S, Devlin B, Kelsoe JR, Sklar P, Daly MJ, O'Donovan MC, Craddock N, Sullivan PF, Smoller JW, Kendler KS, and Wray NR
Subjects: Adult, Attention Deficit Disorder with Hyperactivity genetics, Bipolar Disorder genetics, Child, Child Development Disorders, Pervasive genetics, Crohn Disease genetics, Depressive Disorder, Major genetics, Genetic Heterogeneity, Genome, Human, Humans, Inheritance Patterns, Schizophrenia genetics, Genetic Predisposition to Disease, Genome-Wide Association Study, Mental Disorders genetics, Polymorphism, Single Nucleotide
Abstract: Most psychiatric disorders are moderately to highly heritable. The degree to which genetic variation is unique to individual disorders or shared across disorders is unclear. To examine shared genetic etiology, we use genome-wide genotype data from the Psychiatric Genomics Consortium (PGC) for cases and controls in schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD). We apply univariate and bivariate methods for the estimation of genetic variation within and covariation between disorders. SNPs explained 17-29% of the variance in liability. The genetic correlation calculated using common SNPs was high between schizophrenia and bipolar disorder (0.68 ± 0.04 s.e.), moderate between schizophrenia and major depressive disorder (0.43 ± 0.06 s.e.), bipolar disorder and major depressive disorder (0.47 ± 0.06 s.e.), and ADHD and major depressive disorder (0.32 ± 0.07 s.e.), low between schizophrenia and ASD (0.16 ± 0.06 s.e.) and non-significant for other pairs of disorders as well as between psychiatric disorders and the negative control of Crohn's disease. This empirical evidence of shared genetic etiology for psychiatric disorders can inform nosology and encourages the investigation of common pathophysiologies for related disorders.
Published: 2013
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47. Substance use disorders in adolescents with attention deficit hyperactivity disorder: a 4-year follow-up study.

Author: Groenman AP, Oosterlaan J, Rommelse N, Franke B, Roeyers H, Oades RD, Sergeant JA, Buitelaar JK, and Faraone SV
Subjects: Adolescent, Age of Onset, Attention Deficit Disorder with Hyperactivity epidemiology, Attention Deficit and Disruptive Behavior Disorders epidemiology, Case-Control Studies, Child, Child, Preschool, Conduct Disorder epidemiology, Europe epidemiology, Follow-Up Studies, Humans, Prevalence, Psychotropic Drugs, Risk Factors, Substance-Related Disorders epidemiology, Tobacco Use Disorder epidemiology, Tobacco Use Disorder psychology, Attention Deficit Disorder with Hyperactivity complications, Attention Deficit and Disruptive Behavior Disorders complications, Conduct Disorder complications, Substance-Related Disorders psychology
Abstract: Aim: To examine the relationship between a childhood diagnosis of attention deficit hyperactivity disorder (ADHD) with or without oppositional defiant disorder (ODD)/conduct disorder (CD) and the development of later alcohol/drug use disorder [psychoactive substance use disorder (PSUD)] and nicotine dependence in a large European sample of ADHD probands, their siblings and healthy control subjects., Participants, Design and Setting: Subjects (n = 1017) were participants in the Belgian, Dutch and German part of the International Multicenter ADHD Genetics (IMAGE) study. IMAGE families were identified through ADHD probands aged 5-17 years attending out-patient clinics, and control subjects from the same geographic areas. After a follow-up period (mean: 4.4 years) this subsample was re-assessed at a mean age of 16.4 years., Measurements: PSUD and nicotine dependence were assessed using the Diagnostic Interview Schedule for Children, Alcohol Use Disorders Identification Test, Drug Abuse Screening Test and Fagerström test for Nicotine Dependence., Findings: The ADHD sample was at higher risk of developing PSUD [hazard ratio (HR) = 1.77, 95% confidence interval (CI) = 1.05-3.00] and nicotine dependence (HR = 8.61, 95% CI = 2.44-30.34) than healthy controls. The rates of these disorders were highest for ADHD youth who also had CD, but could not be accounted for by this comorbidity. We did not find an increased risk of developing PSUD (HR = 1.18, 95% CI = 0.62-2.27) or nicotine dependence (HR = 1.89, 95% CI = 0.46-7.77) among unaffected siblings of ADHD youth., Conclusions: A childhood diagnosis of attention deficit hyperactivity disorder is a risk factor for psychoactive substance use disorder and nicotine dependence in adolescence and comorbid conduct disorder, but not oppositional defiant disorder, further increases the risk of developing psychoactive substance use disorder and nicotine dependence., (© 2013 Society for the Study of Addiction.)
Published: 2013
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48. Stimulant treatment for attention-deficit hyperactivity disorder and risk of developing substance use disorder.

Author: Groenman AP, Oosterlaan J, Rommelse NN, Franke B, Greven CU, Hoekstra PJ, Hartman CA, Luman M, Roeyers H, Oades RD, Sergeant JA, Buitelaar JK, and Faraone SV
Subjects: Adolescent, Case-Control Studies, Central Nervous System Stimulants therapeutic use, Child, Female, Follow-Up Studies, Humans, Longitudinal Studies, Male, Prospective Studies, Risk, Substance-Related Disorders diagnosis, Tobacco Use Disorder diagnosis, Attention Deficit Disorder with Hyperactivity drug therapy, Attention Deficit and Disruptive Behavior Disorders drug therapy, Central Nervous System Stimulants adverse effects, Conduct Disorder drug therapy, Substance-Related Disorders etiology, Tobacco Use Disorder etiology
Abstract: Background: Attention-deficit hyperactivity disorder (ADHD) is linked to increased risk for substance use disorders and nicotine dependence., Aims: To examine the effects of stimulant treatment on subsequent risk for substance use disorder and nicotine dependence in a prospective longitudinal ADHD case-control study., Method: At baseline we assessed ADHD, conduct disorder and oppositional defiant disorder. Substance use disorders, nicotine dependence and stimulant treatment were assessed retrospectively after a mean follow-up of 4.4 years, at a mean age of 16.4 years., Results: Stimulant treatment of ADHD was linked to a reduced risk for substance use disorders compared with no stimulant treatment, even after controlling for conduct disorder and oppositional defiant disorder (hazard ratio (HR) = 1.91, 95% CI 1.10-3.36), but not to nicotine dependence (HR = 1.12, 95% CI 0.45-2.96). Within the stimulant-treated group, a protective effect of age at first stimulant use on substance use disorder development was found, which diminished with age, and seemed to reverse around the age of 18., Conclusions: Stimulant treatment appears to lower the risk of developing substance use disorders and does not have an impact on the development of nicotine dependence in adolescents with ADHD.
Published: 2013
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49. A behavioral neuroenergetics theory of ADHD.

Author: Killeen PR, Russell VA, and Sergeant JA
Subjects: Attention physiology, Attention Deficit Disorder with Hyperactivity genetics, Female, Humans, Lactic Acid metabolism, Male, Memory, Short-Term physiology, Norepinephrine physiology, Psychomotor Performance physiology, Receptors, Adrenergic physiology, Attention Deficit Disorder with Hyperactivity physiopathology, Attention Deficit Disorder with Hyperactivity psychology, Energy Metabolism physiology
Abstract: Energetic insufficiency in neurons due to inadequate lactate supply is implicated in several neuropathologies, including attention-deficit/hyperactivity disorder (ADHD). By formalizing the mechanism and implications of such constraints on function, the behavioral Neuroenergetics Theory (NeT) predicts the results of many neuropsychological tasks involving individuals with ADHD and kindred dysfunctions, and entails many novel predictions. The associated diffusion model predicts that response times will follow a mixture of Wald distributions from the attentive state, and ex-Wald distributions after attentional lapses. It is inferred from the model that ADHD participants can bring only 75-85% of the neurocognitive energy to bear on tasks, and allocate only about 85% of the cognitive resources of comparison groups. Parameters derived from the model in specific tasks predict performance in other tasks, and in clinical conditions often associated with ADHD. The primary action of therapeutic stimulants is to increase norepinephrine in active regions of the brain. This activates glial adrenoceptors, increasing the release of lactate from astrocytes to fuel depleted neurons. The theory is aligned with other approaches and integrated with more general theories of ADHD. Therapeutic implications are explored., (Copyright © 2013 Elsevier Ltd. All rights reserved.)
Published: 2013
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50. Comorbid anxiety and neurocognitive dysfunctions in children with ADHD.

Author: Bloemsma JM, Boer F, Arnold R, Banaschewski T, Faraone SV, Buitelaar JK, Sergeant JA, Rommelse N, and Oosterlaan J
Subjects: Adolescent, Anxiety psychology, Attention Deficit Disorder with Hyperactivity psychology, Child, Child, Preschool, Cognition Disorders psychology, Diagnostic and Statistical Manual of Mental Disorders, Executive Function physiology, Female, Humans, Inhibition, Psychological, Male, Neuropsychological Tests, Reaction Time physiology, Severity of Illness Index, Young Adult, Anxiety complications, Attention Deficit Disorder with Hyperactivity complications, Cognition Disorders complications
Abstract: Previous research established that children with ADHD and comorbid anxiety have a later age of ADHD onset, show less off-task and hyperactive behavior, and have more school problems than children with ADHD alone. Comorbid anxiety appears to ameliorate behavioral inhibition deficits, worsen working memory problems, and lengthen reaction times in ADHD. This study investigated the effect of comorbid anxiety on a broad range of neurocognitive functions and includes child-, parent- and teacher reports of anxiety. The sample consisted of 509 children in the age range 5-19 years, including 238 children with a diagnosis of ADHD combined subtype and 271 normal control children. Children were tested on a broad battery of neurocognitive tasks that proved highly sensitive to ADHD in previous work. Linear Structural Equation Modeling (SEM) was used to estimate the effect of comorbid anxiety on the neurocognitive functions. Child reported anxiety was associated with slower motor speed and response speed and better behavioral inhibition. Teacher reported anxiety was related to worse time production. Parent reported anxiety was not significantly associated with any of the neurocognitive functions. Compared to parent and teacher reports of anxiety, child reported comorbid anxiety shows foremost the largest associations with the neurocognitive dysfunctions observed in children with ADHD. This stresses the importance of including child self-reported anxiety assessments in clinical and research practice.
Published: 2013
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