@article{EsserWyschkon2001, author = {Esser, G{\"u}nter and Wyschkon, Anne}, title = {17 Jahre danach : was wird aus Kindern mit Legasthenie?}, year = {2001}, language = {de} } @article{WyschkonSchulzGallitetal.2017, author = {Wyschkon, Anne and Schulz, Franziska and Gallit, Finja Sunnyi and Poltz, Nadine and Kohn-Henkel, Juliane and Moraske, Svenja and Bond{\"u}, Rebecca and von Aster, Michael G. and Esser, G{\"u}nter}, title = {5-Jahres-Verlauf der LRS}, series = {Zeitschrift f{\"u}r Kinder- und Jugendpsychiatrie und Psychotherapie}, volume = {46}, journal = {Zeitschrift f{\"u}r Kinder- und Jugendpsychiatrie und Psychotherapie}, number = {2}, publisher = {Hogrefe}, address = {Bern}, issn = {1422-4917}, doi = {10.1024/1422-4917/a000535}, pages = {107 -- 122}, year = {2017}, abstract = {Fragestellung: Untersucht wird der Verlauf von Kindern mit Lese-Rechtschreibst{\"o}rungen (LRS) {\"u}ber gut 5 Jahre unter Ber{\"u}cksichtigung des Einflusses des Geschlechts der Betroffenen. Außerdem werden Auswirkungen der LRS auf das sp{\"a}tere Schriftsprachniveau und den Schulerfolg {\"u}berpr{\"u}ft. Methodik: Eingangs wurden 995 Sch{\"u}ler zwischen 6 und 16 Jahren untersucht. Ein Teil dieser Kinder ist nach 43 sowie 63 Monaten nachuntersucht worden. Eine LRS wurde diagnostiziert, wenn f{\"u}r das Lesen bzw. Rechtschreiben das doppelte Diskrepanzkriterium von 1.5 Standardabweichungen zur nonverbalen Intelligenz und dem Mittelwert der Klassenstufe erf{\"u}llt war und gleichzeitig keine Minderbegabung vorlag. Ergebnisse: Die LRS weist {\"u}ber einen Zeitraum von 63 Monaten eine hohe St{\"o}rungspersistenz von knapp 70 \% auf. Der 5-Jahres-Verlauf der mittleren Lese- und Rechtschreibleistungen wurde nicht vom Geschlecht beeinflusst. Trotz durchschnittlicher Intelligenz blieben die LRS-Sch{\"u}ler in der Schriftsprache mindestens eine Standardabweichung hinter durchschnittlich und etwa 0.5 Standardabweichungseinheiten hinter unterdurchschnittlich intelligenten Kindern zur{\"u}ck. Der Schulerfolg der LRS-Sch{\"u}ler glich dem unterdurchschnittlich intelligenter Kinder und fiel deutlich schlechter aus als bei durchschnittlich intelligenten Kontrollkindern. Schlussfolgerungen: Eine LRS stellt ein erhebliches Entwicklungsrisiko dar, was fr{\"u}hzeitige Diagnostik- und Therapiemaßnahmen erfordert. Daf{\"u}r sind reliable und im Hinblick auf die resultierenden Pr{\"a}valenzraten sinnvolle, allgemein anerkannte Diagnosekriterien essenziell.}, language = {de} } @article{KuhlmannBuergerEsseretal.2015, author = {Kuhlmann, Sophie Merle and B{\"u}rger, Arne and Esser, G{\"u}nter and Hammerle, Florian}, title = {A mindfulness-based stress prevention training for medical students (MediMind): study protocol for a randomized controlled trial}, series = {Trials}, volume = {16}, journal = {Trials}, publisher = {BioMed Central}, address = {London}, issn = {1745-6215}, doi = {10.1186/s13063-014-0533-9}, pages = {11}, year = {2015}, abstract = {Background: Medical training is very demanding and associated with a high prevalence of psychological distress. Compared to the general population, medical students are at a greater risk of developing a psychological disorder. Various attempts of stress management training in medical school have achieved positive results on minimizing psychological distress; however, there are often limitations. Therefore, the use of a rigorous scientific method is needed. The present study protocol describes a randomized controlled trial to examine the effectiveness of a specifically developed mindfulness-based stress prevention training for medical students that includes selected elements of cognitive behavioral strategies (MediMind). Methods/Design: This study protocol presents a prospective randomized controlled trial, involving four assessment time points: baseline, post-intervention, one-year follow-up and five-year follow-up. The aims include evaluating the effect on stress, coping, psychological morbidity and personality traits with validated measures. Participants are allocated randomly to one of three conditions: MediMind, Autogenic Training or control group. Eligible participants are medical or dental students in the second or eighth semester of a German university. They form a population of approximately 420 students in each academic term. A final total sample size of 126 (at five-year follow-up) is targeted. The trainings (MediMind and Autogenic Training) comprise five weekly sessions lasting 90 minutes each. MediMind will be offered to participants of the control group once the five-year follow-up is completed. The allotment is randomized with a stratified allocation ratio by course of studies, semester, and gender. After descriptive statistics have been evaluated, inferential statistical analysis will be carried out with a repeated measures ANOVA-design with interactions between time and group. Effect sizes will be calculated using partial.-square values. Discussion: Potential limitations of this study are voluntary participation and the risk of attrition, especially concerning participants that are allocated to the control group. Strengths are the study design, namely random allocation, follow-up assessment, the use of control groups and inclusion of participants at different stages of medical training with the possibility of differential analysis.}, language = {en} } @article{EsserIhle2008, author = {Esser, G{\"u}nter and Ihle, Wolfgang}, title = {Abh{\"a}ngigkeit von legalen und illegalen psychotropen Substanzen}, year = {2008}, language = {de} } @article{Esser2002, author = {Esser, G{\"u}nter}, title = {Ablehnung und Vernachl{\"a}ssigung von S{\"a}uglingen}, year = {2002}, language = {de} } @article{KohnEsser2008, author = {Kohn, Juliane and Esser, G{\"u}nter}, title = {ADHS im Jugend- und Erwachsenenalter}, issn = {0026-9298}, doi = {10.1007/s00112-008-1731-x}, year = {2008}, language = {de} } @article{IhleEsserSchmidt2005, author = {Ihle, Wolfgang and Esser, G{\"u}nter and Schmidt, M. H.}, title = {Aggressiv-dissoziale St{\"o}rungen und rechtsextreme Einstellungen : Pr{\"a}valenz, Geschlechtsunterschiede, Verlauf und Risikofaktoren}, year = {2005}, language = {de} } @article{HeinrichBuchmannZohseletal.2015, author = {Heinrich, Angela and Buchmann, Arlette F. and Zohsel, Katrin and Dukal, Helene and Frank, Josef and Treutlein, Jens and Nieratschker, Vanessa and Witt, Stephanie H. and Brandeis, Daniel and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Laucht, Manfred and Rietschel, Marcella}, title = {Alterations of Glucocorticoid Receptor Gene Methylation in Externalizing Disorders During Childhood and Adolescence}, series = {Behavior genetics : an international journal devoted to research in the inheritance of behavior in animals and man}, volume = {45}, journal = {Behavior genetics : an international journal devoted to research in the inheritance of behavior in animals and man}, number = {5}, publisher = {Springer}, address = {New York}, issn = {0001-8244}, doi = {10.1007/s10519-015-9721-y}, pages = {529 -- 536}, year = {2015}, abstract = {Epigenetic modulations are a hypothesized link between environmental factors and the development of psychiatric disorders. Research has suggested that patients with depression or bipolar disorder exhibit higher methylation levels in the glucocorticoid receptor gene NR3C1. We aimed to investigate whether NR3C1 methylation changes are similarly associated with externalizing disorders such as aggressive behavior and conduct disorder. NR3C1 exon 1F methylation was analyzed in young adults with a lifetime diagnosis of an externalizing disorder (N = 68) or a depressive disorder (N = 27) and healthy controls (N = 124) from the Mannheim Study of Children at Risk. The externalizing disorders group had significantly lower NR3C1 methylation levels than the lifetime depressive disorder group (p = 0.009) and healthy controls (p = 0.001) This report of lower methylation levels in NR3C1 in externalizing disorders may indicate a mechanism through which the differential development of externalizing disorders as opposed to depressive disorders might occur.}, language = {en} } @article{WittBuchmannBlomeyeretal.2011, author = {Witt, Stephanie H. and Buchmann, Arlette F. and Blomeyer, Dorothea and Nieratschker, Vanessa and Treutlein, Jens and Esser, G{\"u}nter and Schmidt, Martin H. and Bidlingmaier, Martin and Wiedemann, Klaus and Rietschel, Marcella and Laucht, Manfred and Wuest, Stefan and Zimmermann, Ulrich S.}, title = {An interaction between a neuropeptide Y gene polymorphism and early adversity modulates endocrine stress responses}, series = {Psychoneuroendocrinology}, volume = {36}, journal = {Psychoneuroendocrinology}, number = {7}, publisher = {Elsevier}, address = {Oxford}, issn = {0306-4530}, doi = {10.1016/j.psyneuen.2010.12.015}, pages = {1010 -- 1020}, year = {2011}, abstract = {Interindividual variability in the regulation of the human stress system accounts for a part of the individual's liability to stress-related diseases. These differences are influenced by environmental and genetic factors. Early childhood adversity is a well-studied environmental factor affecting an individual's stress response which has been shown to be modulated by gene environment interaction (GxE). Neuropeptide Y (NPY) plays a role in stress regulation and genetic variation in NPY may influence stress responses. In this study, we analyzed the association of a common variant in the NPY gene promoter, rs16147, with cortisol and ACTH responses to acute psychosocial stress in young adults from the Mannheim Study of Children at Risk (MARS), an ongoing epidemiological cohort study following the outcome of early adversity from birth into adulthood. We found evidence of a GxE interaction between rs16147 and early adversity significantly affecting HPA axis responses to acute psychosocial stress. These findings suggest that the neurobiological mechanisms linking early adverse experience and later neuroendocrine stress regulation are modulated by a gene variant whose functional relevance is documented by increasing convergent evidence from in vitro, animal and human studies.}, language = {en} } @article{IhleEsserSchmidtetal.1999, author = {Ihle, Wolfgang and Esser, G{\"u}nter and Schmidt, Martin H. and Blanz, Bernhard and Reis, Olaf and Meyer-Probst, Bernhard}, title = {Angst als psychosoziales Ph{\"a}nomen und psychotherapeutisches Anliegen}, year = {1999}, language = {de} } @article{Esser1999, author = {Esser, G{\"u}nter}, title = {Anmerkungen zur Kaufmann-Assessment Battery for Children (K-ABC)}, year = {1999}, language = {de} } @article{EsserFreybergerHoffmannetal.2006, author = {Esser, G{\"u}nter and Freyberger, H. J. and Hoffmann, S. O. and Hoyer, J. and Richter, R. and Harfst, T.}, title = {Anpassung der Psychotherapie-Richtlinien zur Zulassung psychotherapeutischer Verfahren und Methoden}, year = {2006}, language = {de} } @article{NikitopoulosZohselBlomeyeretal.2014, author = {Nikitopoulos, Joerg and Zohsel, Katrin and Blomeyer, Dorothea and Buchmann, Arlette F. and Schmid, Brigitte and Jennen-Steinmetz, Christine and Becker, Katja and Schmidt, Martin H. and Esser, G{\"u}nter and Brandeis, Daniel and Banaschewski, Tobias and Laucht, Manfred}, title = {Are infants differentially sensitive to parenting? Early maternal care, DRD4 genotype and externalizing behavior during adolescence}, series = {Journal of psychiatric research}, volume = {59}, journal = {Journal of psychiatric research}, publisher = {Elsevier}, address = {Oxford}, issn = {0022-3956}, doi = {10.1016/j.jpsychires.2014.08.012}, pages = {53 -- 59}, year = {2014}, language = {en} } @article{LauchtHohmEsseretal.2007, author = {Laucht, Manfred and Hohm, E. and Esser, G{\"u}nter and Schmidt, Martin H. and Becker, Katja}, title = {Association between ADHD and smoking in adolescence : shared genetic, environmental and psychopathological factors}, issn = {0300-9564}, doi = {10.1007/s00702-007-0703-y}, year = {2007}, abstract = {The present study aimed to examine the extent to which the co-occurrence of ADHD and smoking in adolescents could be attributed to common genetic, environmental and psychopathological factors. Data are from an ongoing prospective study of the outcome of early risk factors. At age 15 years, 305 adolescents completed self-report questionnaires measuring tobacco consumption and deviant peer affiliations. Lifetime psychiatric diagnoses were obtained using standardized interviews. DNA was genotyped for the dopamine D4 receptor (DRD4) gene exon III polymorphism. Adolescents with a lifetime diagnosis of ADHD displayed significantly higher smoking activity than non-ADHD controls. A major component of this association could be accounted for by deviant peer affiliations and the comorbidity with oppositional-defiant and conduct disorder, while a minor part was attributable to DRD4 in males but not in females. These findings suggest that the association of ADHD with smoking relies on risk factors shared by the two behaviors.}, language = {en} } @article{BoeckerSchlierHolzHohmetal.2017, author = {Boecker-Schlier, Regina and Holz, Nathalie E. and Hohm, Erika and Zohsel, Katrin and Blomeyer, Dorothea and Buchmann, Arlette F. and Baumeister, Sarah and Wolf, Isabella and Esser, G{\"u}nter and Schmidt, Martin H. and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred}, title = {Association between pubertal stage at first drink and neural reward processing in early adulthood}, series = {Addiction biology}, volume = {22}, journal = {Addiction biology}, publisher = {Wiley}, address = {Hoboken}, issn = {1355-6215}, doi = {10.1111/adb.12413}, pages = {1402 -- 1415}, year = {2017}, abstract = {Puberty is a critical time period during human development. It is characterized by high levels of risk-taking behavior, such as increased alcohol consumption, and is accompanied by various neurobiological changes. Recent studies in animals and humans have revealed that the pubertal stage at first drink (PSFD) significantly impacts drinking behavior in adulthood. Moreover, neuronal alterations of the dopaminergic reward system have been associated with alcohol abuse or addiction. This study aimed to clarify the impact of PSFD on neuronal characteristics of reward processing linked to alcohol-related problems. One hundred sixty-eight healthy young adults from a prospective study covering 25 years participated in a monetary incentive delay task measured with simultaneous EEG-fMRI. PSFD was determined according to the age at menarche or Tanner stage of pubertal development, respectively. Alcohol-related problems in early adulthood were assessed with the Alcohol Use Disorder Identification Test (AUDIT). During reward anticipation, decreased fMRI activation of the frontal cortex and increased preparatory EEG activity (contingent negative variation) occurred with pubertal compared to postpubertal first alcohol intake. Moreover, alcohol-related problems during early adulthood were increased in pubertal compared to postpubertal beginners, which was mediated by neuronal activation of the right medial frontal gyrus. At reward delivery, increased fMRI activation of the left caudate and higher feedback-related EEG negativity were detected in pubertal compared to postpubertal beginners. Together with animal findings, these results implicate PSFD as a potential modulator of psychopathology, involving altered reward anticipation. Both PSFD timing and reward processing might thus be potential targets for early prevention and intervention.}, language = {en} } @article{HohmannHohmTreutleinetal.2015, author = {Hohmann, Sarah and Hohm, Erika and Treutlein, Jens and Blomeyer, Dorothea and Jennen-Steinmetz, Christine and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred}, title = {Association of norepinephrine transporter (NET, SLC6A2) genotype with ADHD-related phenotypes: Findings of a longitudinal study from birth to adolescence}, series = {Psychiatry research : the official publication of the International Society for Neuroimaging in Psychiatry}, volume = {226}, journal = {Psychiatry research : the official publication of the International Society for Neuroimaging in Psychiatry}, number = {2-3}, publisher = {Elsevier}, address = {Clare}, issn = {0165-1781}, doi = {10.1016/j.psychres.2014.12.029}, pages = {425 -- 433}, year = {2015}, abstract = {Variation in the gene encoding for the norepinephrine transporter (NET, SLC6A2) has repeatedly been linked with ADHD, although there is some inconsistency regarding the association with specific genes. The variants for which most consistent association has been found are the NET variants rs3785157 and rs28386840. Here, we tested for their association with ADHD diagnosis and ADHD-related phenotypes during development in a longitudinal German community sample. Children were followed from age 4 to age 15, using diagnostic interviews to assess ADHD. Between the ages of 8 and 15 years, the Child Behavior Checklist (CBCL) was administered to the primary caregivers. The continuous performance task (CPT) was performed at age 15. Controlling for possible confounders, we found that homozygous carriers of the major A allele of the functional promoter variant rs28386840 displayed a higher rate of ADHD lifetime diagnosis. Moreover, homozygous carriers of the minor T allele of rs3785157 were more likely to develop ADHD and showed higher scores on the CBCL externalizing behavior scales. Additionally, we found that individuals heterozygous for rs3785157 made fewer omission errors in the CPT than homozygotes. This is the first longitudinal study to report associations between specific NET variants and ADHD-related phenotypes during the course of development. (C) 2015 Elsevier Ireland Ltd. All rights reserved.}, language = {en} } @article{BlomeyerBuchmannLascorzetal.2013, author = {Blomeyer, Dorothea and Buchmann, Arlette F. and Lascorz, Jesus and Zimmermann, Ulrich S. and Esser, G{\"u}nter and Desrivieres, Sylvane and Schmidt, Martin H. and Banaschewski, Tobias and Schumann, Gunter and Laucht, Manfred}, title = {Association of PER2 genotype and stressful life events with alcohol drinking in young adults}, series = {PLoS one}, volume = {8}, journal = {PLoS one}, number = {3}, publisher = {PLoS}, address = {San Fransisco}, issn = {1932-6203}, doi = {10.1371/journal.pone.0059136}, pages = {7}, year = {2013}, abstract = {Background: Clock genes govern circadian rhythms and shape the effect of alcohol use on the physiological system. Exposure to severe negative life events is related to both heavy drinking and disturbed circadian rhythmicity. The aim of this study was 1) to extend previous findings suggesting an association of a haplotype tagging single nucleotide polymorphism of PER2 gene with drinking patterns, and 2) to examine a possible role for an interaction of this gene with life stress in hazardous drinking. Methods: Data were collected as part of an epidemiological cohort study on the outcome of early risk factors followed since birth. At age 19 years, 268 young adults (126 males, 142 females) were genotyped for PER2 rs56013859 and were administered a 45-day alcohol timeline follow-back interview and the Alcohol Use Disorders Identification Test (AUDIT). Life stress was assessed as the number of severe negative life events during the past four years reported in a questionnaire and validated by interview. Results: Individuals with the minor G allele of rs56013859 were found to be less engaged in alcohol use, drinking at only 72\% of the days compared to homozygotes for the major A allele. Moreover, among regular drinkers, a gene x environment interaction emerged (p = .020). While no effects of genotype appeared under conditions of low stress, carriers of the G allele exhibited less hazardous drinking than those homozygous for the A allele when exposed to high stress. Conclusions: These findings may suggest a role of the circadian rhythm gene PER2 in both the drinking patterns of young adults and in moderating the impact of severe life stress on hazardous drinking in experienced alcohol users. However, in light of the likely burden of multiple tests, the nature of the measures used and the nominal evidence of interaction, replication is needed before drawing firm conclusions.}, language = {en} } @article{WeindrichJennenSteinmetzLauchtetal.1998, author = {Weindrich, D. and Jennen-Steinmetz, Christine and Laucht, Manfred and Esser, G{\"u}nter and Schmidt, Martin H.}, title = {At risk for language disorders? : correlates and course of language disorders in preschool children born at risk}, issn = {0803-5253}, year = {1998}, language = {en} } @article{LangeEsser2005, author = {Lange, Sabine and Esser, G{\"u}nter}, title = {Auditiv-sprachliche St{\"o}rung der Informationsverarbeitung bei Lese-Rechtschreib-St{\"o}rung.}, isbn = {3-89967-220-8}, year = {2005}, language = {de} } @article{HirschbergerEsser2005, author = {Hirschberger, E. and Esser, G{\"u}nter}, title = {Auditive selektive Aufmerksamkeit bei geriatrischen Patienten mit einem visuellen Neglect}, isbn = {3-89967-220-8}, year = {2005}, language = {de} }