Suchergebnisse

International audience ; Advanced paternal age has been consistently associated with an increased risk of schizophrenia. It is less known if such an association also exists with subclinical/attenuated forms of psychosis. Additionally, it has been suggested that it is not paternal age per se, but rather delayed fatherhood, as a marker of a genetic liability of psychosis, that is the cause of the association. The aim of the current study was to examine whether paternal age and/or delayed fatherhood (paternity age) predict self-reported positive, negative, and/or depressive dimensions of psychosis in a large sample from the general population. The sample (N = 1465) was composed of control subjects from the 6 countries participating in the European Union Gene-Environment Interaction study. The CAPE, a self-report questionnaire, was used to measure dimensions of subclinical psychosis. Paternal age at the time of respondents' birth and age of paternity were assessed by self-report. We assessed the influence of the variables of interest (paternal age or paternity age) on CAPE scores after adjusting for potential confounders (age, gender, and ethnicity). Paternal age was positively associated with the positive dimension of the CAPE. By contrast, paternity age was not associated with any of the psychosis dimensions assessed by the CAPE. Thus, our results do not support the idea that delayed fatherhood explains the association between age of paternity and psychosis risk. Furthermore, our results provide arguments for the hypothesis of an etiologic continuum of psychosis.

International audience ; Advanced paternal age has been consistently associated with an increased risk of schizophrenia. It is less known if such an association also exists with subclinical/attenuated forms of psychosis. Additionally, it has been suggested that it is not paternal age per se, but rather delayed fatherhood, as a marker of a genetic liability of psychosis, that is the cause of the association. The aim of the current study was to examine whether paternal age and/or delayed fatherhood (paternity age) predict self-reported positive, negative, and/or depressive dimensions of psychosis in a large sample from the general population. The sample (N = 1465) was composed of control subjects from the 6 countries participating in the European Union Gene-Environment Interaction study. The CAPE, a self-report questionnaire, was used to measure dimensions of subclinical psychosis. Paternal age at the time of respondents' birth and age of paternity were assessed by self-report. We assessed the influence of the variables of interest (paternal age or paternity age) on CAPE scores after adjusting for potential confounders (age, gender, and ethnicity). Paternal age was positively associated with the positive dimension of the CAPE. By contrast, paternity age was not associated with any of the psychosis dimensions assessed by the CAPE. Thus, our results do not support the idea that delayed fatherhood explains the association between age of paternity and psychosis risk. Furthermore, our results provide arguments for the hypothesis of an etiologic continuum of psychosis.

International audience ; Advanced paternal age has been consistently associated with an increased risk of schizophrenia. It is less known if such an association also exists with subclinical/attenuated forms of psychosis. Additionally, it has been suggested that it is not paternal age per se, but rather delayed fatherhood, as a marker of a genetic liability of psychosis, that is the cause of the association. The aim of the current study was to examine whether paternal age and/or delayed fatherhood (paternity age) predict self-reported positive, negative, and/or depressive dimensions of psychosis in a large sample from the general population. The sample (N = 1465) was composed of control subjects from the 6 countries participating in the European Union Gene-Environment Interaction study. The CAPE, a self-report questionnaire, was used to measure dimensions of subclinical psychosis. Paternal age at the time of respondents' birth and age of paternity were assessed by self-report. We assessed the influence of the variables of interest (paternal age or paternity age) on CAPE scores after adjusting for potential confounders (age, gender, and ethnicity). Paternal age was positively associated with the positive dimension of the CAPE. By contrast, paternity age was not associated with any of the psychosis dimensions assessed by the CAPE. Thus, our results do not support the idea that delayed fatherhood explains the association between age of paternity and psychosis risk. Furthermore, our results provide arguments for the hypothesis of an etiologic continuum of psychosis.

Advanced paternal age has been consistently associated with an increased risk of schizophrenia. It is less known if such an association also exists with subclinical/attenuated forms of psychosis. Additionally, it has been suggested that it is not paternal age per se, but rather delayed fatherhood, as a marker of a genetic liability of psychosis, that is the cause of the association. The aim of the current study was to examine whether paternal age and/or delayed fatherhood (paternity age) predict self-reported positive, negative, and/or depressive dimensions of psychosis in a large sample from the general population. The sample (N = 1465) was composed of control subjects from the 6 countries participating in the European Union Gene-Environment Interaction study. The CAPE, a self-report questionnaire, was used to measure dimensions of subclinical psychosis. Paternal age at the time of respondents' birth and age of paternity were assessed by self-report. We assessed the influence of the variables of interest (paternal age or paternity age) on CAPE scores after adjusting for potential confounders (age, gender, and ethnicity). Paternal age was positively associated with the positive dimension of the CAPE. By contrast, paternity age was not associated with any of the psychosis dimensions assessed by the CAPE. Thus, our results do not support the idea that delayed fatherhood explains the association between age of paternity and psychosis risk. Furthermore, our results provide arguments for the hypothesis of an etiologic continuum of psychosis.

Objective. To test for differences in reported age at onset (AAO) of bipolar I affective disorder in clinical samples drawn from Europe and the USA. Methods. Admixture analysis was used to identify the model best fitting the observed AAO distributions of two large samples of bipolar I patients from Europe and USA (n = 3616 and n = 2275, respectively). Theoretical AAO functions were compared between the two samples. Results. The model best fitting the observed distribution of AAO in both samples was a mixture of three Gaussian distributions. The theoretical AAO functions of bipolar I disorder differed significantly between the European and USA populations, with further analyses indicating that (i) the proportion of patients belonging to the early-onset subgroup was higher in the USA sample (63 vs. 25%) and (ii) mean age at onset (±SD) in the early-onset subgroup was lower for the USA sample (14.5 ± 4.9 vs. 19 ± 2.7 years). Conclusions. The models best describing the reported AAO distributions of European and USA bipolar I patients were remarkably stable. The intermediate- and late-onset subgroups had similar characteristics in the two samples. However, the theoretical AAO function differed significantly between the USA and European samples due to the higher proportion of patients in the early-onset subgroup and the lower mean age-at-onset in the USA sample.

Despite the high impact of mental disorders in society, European mental health research is at a critical situation with a relatively low level of funding, and few advances been achieved during the last decade. The development of coordinated research policies and integrated research networks in mental health is lagging behind other disciplines in Europe, resulting in lower degree of cooperation and scientific impact. To reduce more efficiently the burden of mental disorders in Europe, a concerted new research agenda is necessary. The ROAMER (Roadmap for Mental Health Research in Europe) project, funded under the European Commission's Seventh Framework Programme, aims to develop a comprehensive and integrated mental health research agenda within the perspective of the European Union (EU) Horizon 2020 programme, with a translational goal, covering basic, clinical and public health research. ROAMER covers six major domains: infrastructures and capacity building, biomedicine, psychological research and treatments, social and economic issues, public health and well-being. Within each of them, state-of-the-art and strength, weakness and gap analyses were conducted before building consensus on future research priorities. The process is inclusive and participatory, incorporating a wide diversity of European expert researchers as well as the views of service users, carers, professionals and policy and funding institutions.

Despite the high impact of mental disorders in society, European mental health research is at a critical situation with a relatively low level of funding, and few advances been achieved during the last decade. The development of coordinated research policies and integrated research networks in mental health is lagging behind other disciplines in Europe, resulting in lower degree of cooperation and scientific impact. To reduce more efficiently the burden of mental disorders in Europe, a concerted new research agenda is necessary. The ROAMER (Roadmap for Mental Health Research in Europe) project, funded under the European Commission's Seventh Framework Programme, aims to develop a comprehensive and integrated mental health research agenda within the perspective of the European Union (EU) Horizon 2020 programme, with a translational goal, covering basic, clinical and public health research. ROAMER covers six major domains: infrastructures and capacity building, biomedicine, psychological research and treatments, social and economic issues, public health and well‐being. Within each of them, state‐of‐the‐art and strength, weakness and gap analyses were conducted before building consensus on future research priorities. The process is inclusive and participatory, incorporating a wide diversity of European expert researchers as well as the views of service users, carers, professionals and policy and funding institutions. Copyright © 2013 John Wiley & Sons, Ltd.

The direct estimation of heritability from genome-wide common variant data as implemented in the program Genome-wide Complex Trait Analysis (GCTA) has provided a means to quantify heritability attributable to all interrogated variants. We have quantified the variance in liability to disease explained by all SNPs for two phenotypically-related neurobehavioral disorders, obsessive-compulsive disorder (OCD) and Tourette Syndrome (TS), using GCTA. Our analysis yielded a heritability point estimate of 0.58 (se = 0.09, p = 5.64e-12) for TS, and 0.37 (se = 0.07, p = 1.5e-07) for OCD. in addition, we conducted multiple genomic partitioning analyses to identify genomic elements that concentrate this heritability. We examined genomic architectures of TS and OCD by chromosome, MAF bin, and functional annotations. in addition, we assessed heritability for early onset and adult onset OCD. Among other notable results, we found that SNPs with a minor allele frequency of less than 5% accounted for 21% of the TS heritability and 0% of the OCD heritability. Additionally, we identified a significant contribution to TS and OCD heritability by variants significantly associated with gene expression in two regions of the brain (parietal cortex and cerebellum) for which we had available expression quantitative trait loci (eQTLs). Finally we analyzed the genetic correlation between TS and OCD, revealing a genetic correlation of 0.41 (se = 0.15, p = 0.002). These results are very close to previous heritability estimates for TS and OCD based on twin and family studies, suggesting that very little, if any, heritability is truly missing (i.e., unassayed) from TS and OCD GWAS studies of common variation. the results also indicate that there is some genetic overlap between these two phenotypically-related neuropsychiatric disorders, but suggest that the two disorders have distinct genetic architectures. ; Judah Foundation ; NIH ; Tourette Syndrome Association International Consortium for Genetics (TSAICG) ; New Jersey Center for Tourette Syndrome and Associated Disorders ; NIMH ; Obsessive Compulsive Foundation ; Ontario Mental Health Foundation ; Tourette Syndrome Association ; American Academy of Child and Adolescent Psychiatry (AACAP) ; Anxiety Disorders Association of America (ADAA) ; University of British Columbia ; Michael Smith Foundation ; American Recovery and Re-investment Act (ARRA) ; Australian Research Council ; Australian National Health and Medical Research Council ; German Research Foundation ; NIH Genes, Environment and Health Initiative [GEI] ; Gene Environment Association Studies (GENEVA) under GEI ; NIH GEI ; National Institute on Alcohol Abuse and Alcoholism ; National Institute on Drug Abuse ; Univ Chicago, Dept Med, Med Genet Sect, Chicago, IL 60637 USA ; Harvard Univ, Massachusetts Gen Hosp, Dept Psychiat,Sch Med, Psychiat & Neurodev Genet Unit,Ctr Human Genet Re, Boston, MA USA ; Broad Inst Harvard & MIT, Stanley Ctr Psychiat Res, Cambridge, MA USA ; Univ Chicago, Dept Med, Chicago, IL 60637 USA ; Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA ; Univ Amsterdam, Acad Med Ctr, Dept Psychiat, NL-1105 AZ Amsterdam, Netherlands ; Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA ; Univ Queensland, Diamantina Inst, Brisbane, Qld 4072, Australia ; Univ Queensland, Queensland Brain Inst, Brisbane, Qld 4072, Australia ; Univ Hlth Network, Toronto Western Res Inst, Toronto, ON, Canada ; Hosp Sick Children, Toronto, ON M5G 1X8, Canada ; Univ Vita Salute San Raffaele, Milan, Italy ; Hadassah Hebrew Univ Med Ctr, Herman Dana Div Child & Adolescent Psychiat, Jerusalem, Israel ; Univ Pontificia Bolivariana, Univ Antioquia, Medellin, Colombia ; Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA ; Yale Univ, Dept Psychiat, New Haven, CT 06520 USA ; Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA ; North Shore Long Isl Jewish Med Ctr, Manhasset, NY USA ; NYU Med Ctr, New York, NY 10016 USA ; North Shore Long Isl Jewish Hlth Syst, Manhasset, NY USA ; Hofstra Univ, Sch Med, Hempstead, NY 11550 USA ; Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Mexico City, DF, Mexico ; UCL, London, England ; Univ Hong Kong, Dept Psychiat, Hong Kong, Hong Kong, Peoples R China ; Univ São Paulo, Sch Med, Dept Psychiat, São Paulo, Brazil ; Vrije Univ Amsterdam, Med Ctr, Dept Psychiat, Amsterdam, Netherlands ; Univ Utrecht, Dept Clin & Hlth Psychol, Utrecht, Netherlands ; Altrecht Acad Anxiety Ctr, Utrecht, Netherlands ; Univ Milan, Osped San Raffaele, I-20127 Milan, Italy ; Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA ; Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA ; Univ Montreal, Montreal, PQ, Canada ; Univ Calif Los Angeles, Keck Sch Med, Div Biostat, Dept Preventat Med, Los Angeles, CA USA ; Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60612 USA ; Univ Ghent, Lab Pharmaceut Biotechnol, B-9000 Ghent, Belgium ; Inst Pasteur, Paris, France ; French Natl Sci Fdn, Fondat Fondamental, Creteil, France ; Hop Robert Debre, AP HP, Dept Child & Adolescent Psychiat, F-75019 Paris, France ; Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada ; Univ Wurzburg, Dept Child & Adolescent Psychiat Psychosomat & Ps, D-97070 Wurzburg, Germany ; Univ Munich, Dept Psychiat & Psychotherapy, Munich, Germany ; Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA ; Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp,OCD Program, Boston, MA 02115 USA ; Univ Med Greifswald, Helios Hosp Stralsund, Dept Psychiat & Psychotherapy, Greifswald, Germany ; Butler Hosp, Brown Med Sch, Dept Psychiat & Human Behav, Providence, RI 02906 USA ; Shaare Zedek Med Ctr, Neuropediatr Unit, Jerusalem, Israel ; Rutgers State Univ, Dept Genet, Human Genet Inst New Jersey, Piscataway, NJ USA ; Univ Stellenbosch, Dept Psychiat, ZA-7600 Stellenbosch, South Africa ; Univ São Paulo, Fac Med, Dept Psychiat, BR-05508 São Paulo, Brazil ; Baylor Coll Med, Dept Neurol, Parkinsons Dis Ctr, Houston, TX 77030 USA ; Baylor Coll Med, Dept Neurol, Movement Disorders Clin, Houston, TX 77030 USA ; Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA ; Ctr Addict & Mental Hlth, Neurogenet Sect, Toronto, ON, Canada ; Univ Toronto, Dept Psychiat, Toronto, ON, Canada ; Yale Univ, Sch Med, Dept Genet, Yale Child Study Ctr, New Haven, CT 06510 USA ; Overlook Hosp, Atlantic Neurosci Inst, Summit, NJ USA ; Carracci Med Grp, Mexico City, DF, Mexico ; Inst Mondor Rech Biomed, Creteil, France ; Yale Univ, Ctr Child Study, New Haven, CT 06520 USA ; Univ Bonn, Dept Psychiat & Psychotherapy, Bonn, Germany ; Univ Illinois, Dept Psychiat, Inst Human Genet, Chicago, IL 60612 USA ; Univ Stellenbosch, Dept Psychiat, MRC Unit Anxiety & Stress Disorders, ZA-7600 Stellenbosch, South Africa ; Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA ; UCI, Sch Med, Dept Psychiat & Human Behav, Irvine, CA USA ; Univ Utah, Salt Lake City, UT USA ; NIMH Intramural Res Program, Clin Sci Lab, Bethesda, MD USA ; Med City Dallas Hosp, Dept Clin Res, Dallas, TX USA ; Univ Med Ctr, Rudolf Magnus Inst Neurosci, Dept Psychiat, Utrecht, Netherlands ; Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Ctr Neurobehav Genet, Los Angeles, CA 90024 USA ; Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA ; Univ So Calif, Keck Sch Med, Zilkha Neurogenet Inst, Dept Psychiat & Behav Sci, Los Angeles, CA 90033 USA ; Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA ; Yale Univ, Dept Psychol, New Haven, CT 06520 USA ; Partners Psychiat & McLean Hosp, Boston, MA USA ; Sunnybrook Hlth Sci Ctr, Frederick W Thompson Anxiety Disorders Ctr, Toronto, ON M4N 3M5, Canada ; St George Hosp, London, England ; Sch Med, London, England ; Hosp Nacl Ninos Dr Carlos Saenz Herrera, San Jose, Costa Rica ; Universidade Federal de São Paulo, Dept Psychiat, Child & Adolescent Psychiat Unit UPIA, São Paulo, Brazil ; Wayne State Univ, Dept Psychiat & Behav Neurosci, Detroit, MI 48207 USA ; Detroit Med Ctr, Detroit, MI USA ; McGill Univ, Montreal Neurol Inst, Montreal, PQ, Canada ; Univ Cologne, Dept Psychiat & Psychotherapy, D-50931 Cologne, Germany ; Univ Fed Bahia, Univ Hlth Care Serv SMURB, Salvador, BA, Brazil ; Youthdale Treatment Ctr, Toronto, ON, Canada ; Johns Hopkins Univ Sch Med, Baltimore, MD USA ; Univ Cape Town, ZA-7925 Cape Town, South Africa ; Univ Med Ctr Utrecht, Dept Med Genet, Utrecht, Netherlands ; Vanderbilt Univ, Kennedy Ctr Res Human Dev, Dept Psychiat, Nashville, TN 37235 USA ; Vanderbilt Univ, Kennedy Ctr Res Human Dev, Dept Pediat & Pharmacol, Nashville, TN 37235 USA ; Vanderbilt Univ, Inst Brain, Nashville, TN 37235 USA ; Univ Zurich, Dept Child & Adolescent Psychiat, Zurich, Switzerland ; Univ Wurzburg, Dept Child & Adolescent Psychiat, D-97070 Wurzburg, Germany ; Univ Amsterdam, Acad Med Ctr, Ctr Psychiat, NL-1105 BC Amsterdam, Netherlands ; Inst Royal Netherlands Acad Arts & Sci NIN KNAW, Netherlands Inst Neurosci, Amsterdam, Netherlands ; NIMH Intramural Res Program, Unit Stat Genom, Bethesda, MD USA ; Univ Utah, Dept Psychiat, Salt Lake City, UT USA ; Natl Inst Genom Med SAP, Carracci Med Grp, Mexico City, DF, Mexico ; Vrije Univ Amsterdam, Ctr Neurogen & Cognit Res, Dept Funct Genom, Amsterdam, Netherlands ; Vrije Univ Amsterdam Med Ctr, Dept Clin Genet, Amsterdam, Netherlands ; Erasmus Univ, Med Ctr, Dept Child & Adolescent Psychiat, Rotterdam, Netherlands ; Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA ; Vrije Univ Amsterdam, Med Ctr, Dept Clin Genet, Sect Med Genom, Amsterdam, Netherlands ; German Ctr Neurodegenerat Dis, Tubingen, Germany ; Hosp Sick Children, Program Genet & Genome Biol, Toronto, ON M5G 1X8, Canada ; Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands ; Univ British Columbia, British Columbia Mental Hlth & Addict Res Inst, Vancouver, BC V5Z 1M9, Canada ; Brigham & Womens Hosp, Div Cognit & Behav Neurol, Boston, MA 02115 USA ; Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA ; Universidade Federal de São Paulo, Dept Psychiat, Child & Adolescent Psychiat Unit UPIA, São Paulo, Brazil ; NIH: NS40024 ; NIH: NS16648 ; NIH: MH079489 ; NIH: MH073250 ; NIH: NS037484 ; NIH: 1R01MH079487-01A1 ; NIH: K20 MH01065 ; NIH: R01 MH58376 ; NIH: MH085057 ; NIH: MH079494 ; NIH: HHSN268200782096C ; NIMH: R01MH092293 ; American Recovery and Re-investment Act (ARRA): NS40024-07S1 ; American Recovery and Re-investment Act (ARRA): NS16648-29S1 ; Australian Research Council: FT0991360 ; Australian Research Council: DE130100614 ; Australian National Health and Medical Research Council: 1047956 ; Australian National Health and Medical Research Council: 1052684 ; German Research Foundation: DFG GR 1912/1-1 ; NIH Genes, Environment and Health Initiative [GEI]: U01 HG004422 ; NIH GEI: U01HG004438 ; : R01 MH090937 ; : P50MH094267 ; Web of Science