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The relationship between the recognition of specific basic emotions and negative symptom domains in patients with schizophrenia spectrum disorders
- M. Zierhut, K. Boege, N. Bergmann, I. Hahne, A. Braun, J. Kraft, T.M.T. Ta, S. Ripke, M. Bajbouj, E. Hahn
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- Journal:
- European Psychiatry / Volume 65 / Issue S1 / June 2022
- Published online by Cambridge University Press:
- 01 September 2022, pp. S107-S108
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Introduction
Current research suggests emotion recognition to be significantly impaired in individuals with schizophrenia spectrum disorders (SSD), whereby negative symptoms are theorised to play a crucial role. Emotion recognition deficits are assumed to be predictors of transition from clinical high risk to schizophrenia. So far, little attention has been given hereby to the subdomains of negative symptoms and recognizing the individual basic emotions.
ObjectivesOur study aimed to explore the relationship between the recognition of the basic emotions and each negative symptom domain.
Methods66 patients with a SSD diagnosis were recruited at the Charité – Universitätsmedizin Berlin. Correlational and regression analyses to control for the covariates (age, education, sex) were conducted between the recognition of the six basic emotions (anger, disgust, fear, happiness, sadness, surprise) using the Emotion Recognition Task of the Cambridge Neuropsychological Test Automated Battery (CANTAB) and the seven different subdomains of negative symptoms of the Positive and Negative Syndrome Scale (PANSS).
Resultsrevealed significantly negative correlations of blunted affect with the recognition of happiness, fear, and disgust. Difficulties in abstract thinking, also correlated positively with the recognition of fear. Additionally, we found a significant positive correlation between stereotyped thinking and difficulties in abstract thinking with the response latency in emotion recognition.
ConclusionsIndividuals with SSD and domains of negative symptoms showed specific impairments in recognizing the representation of basic emotions. A longitudinal design to make causality statements would be useful for future research. Moreover, emotion recognition should be considered for early detection and individualized treatment.
DisclosureNo significant relationships.
Characterisation of age and polarity at onset in bipolar disorder
- Janos L. Kalman, Loes M. Olde Loohuis, Annabel Vreeker, Andrew McQuillin, Eli A. Stahl, Douglas Ruderfer, Maria Grigoroiu-Serbanescu, Georgia Panagiotaropoulou, Stephan Ripke, Tim B. Bigdeli, Frederike Stein, Tina Meller, Susanne Meinert, Helena Pelin, Fabian Streit, Sergi Papiol, Mark J. Adams, Rolf Adolfsson, Kristina Adorjan, Ingrid Agartz, Sofie R. Aminoff, Heike Anderson-Schmidt, Ole A. Andreassen, Raffaella Ardau, Jean-Michel Aubry, Ceylan Balaban, Nicholas Bass, Bernhard T. Baune, Frank Bellivier, Antoni Benabarre, Susanne Bengesser, Wade H Berrettini, Marco P. Boks, Evelyn J. Bromet, Katharina Brosch, Monika Budde, William Byerley, Pablo Cervantes, Catina Chillotti, Sven Cichon, Scott R. Clark, Ashley L. Comes, Aiden Corvin, William Coryell, Nick Craddock, David W. Craig, Paul E. Croarkin, Cristiana Cruceanu, Piotr M. Czerski, Nina Dalkner, Udo Dannlowski, Franziska Degenhardt, Maria Del Zompo, J. Raymond DePaulo, Srdjan Djurovic, Howard J. Edenberg, Mariam Al Eissa, Torbjørn Elvsåshagen, Bruno Etain, Ayman H. Fanous, Frederike Fellendorf, Alessia Fiorentino, Andreas J. Forstner, Mark A. Frye, Janice M. Fullerton, Katrin Gade, Julie Garnham, Elliot Gershon, Michael Gill, Fernando S. Goes, Katherine Gordon-Smith, Paul Grof, Jose Guzman-Parra, Tim Hahn, Roland Hasler, Maria Heilbronner, Urs Heilbronner, Stephane Jamain, Esther Jimenez, Ian Jones, Lisa Jones, Lina Jonsson, Rene S. Kahn, John R. Kelsoe, James L. Kennedy, Tilo Kircher, George Kirov, Sarah Kittel-Schneider, Farah Klöhn-Saghatolislam, James A. Knowles, Thorsten M. Kranz, Trine Vik Lagerberg, Mikael Landen, William B. Lawson, Marion Leboyer, Qingqin S. Li, Mario Maj, Dolores Malaspina, Mirko Manchia, Fermin Mayoral, Susan L. McElroy, Melvin G. McInnis, Andrew M. McIntosh, Helena Medeiros, Ingrid Melle, Vihra Milanova, Philip B. Mitchell, Palmiero Monteleone, Alessio Maria Monteleone, Markus M. Nöthen, Tomas Novak, John I. Nurnberger, Niamh O'Brien, Kevin S. O'Connell, Claire O'Donovan, Michael C. O'Donovan, Nils Opel, Abigail Ortiz, Michael J. Owen, Erik Pålsson, Carlos Pato, Michele T. Pato, Joanna Pawlak, Julia-Katharina Pfarr, Claudia Pisanu, James B. Potash, Mark H Rapaport, Daniela Reich-Erkelenz, Andreas Reif, Eva Reininghaus, Jonathan Repple, Hélène Richard-Lepouriel, Marcella Rietschel, Kai Ringwald, Gloria Roberts, Guy Rouleau, Sabrina Schaupp, William A Scheftner, Simon Schmitt, Peter R. Schofield, K. Oliver Schubert, Eva C. Schulte, Barbara Schweizer, Fanny Senner, Giovanni Severino, Sally Sharp, Claire Slaney, Olav B. Smeland, Janet L. Sobell, Alessio Squassina, Pavla Stopkova, John Strauss, Alfonso Tortorella, Gustavo Turecki, Joanna Twarowska-Hauser, Marin Veldic, Eduard Vieta, John B. Vincent, Wei Xu, Clement C. Zai, Peter P. Zandi, Psychiatric Genomics Consortium (PGC) Bipolar Disorder Working Group, International Consortium on Lithium Genetics (ConLiGen), Colombia-US Cross Disorder Collaboration in Psychiatric Genetics, Arianna Di Florio, Jordan W. Smoller, Joanna M. Biernacka, Francis J. McMahon, Martin Alda, Bertram Müller-Myhsok, Nikolaos Koutsouleris, Peter Falkai, Nelson B. Freimer, Till F.M. Andlauer, Thomas G. Schulze, Roel A. Ophoff
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- Journal:
- The British Journal of Psychiatry / Volume 219 / Issue 6 / December 2021
- Published online by Cambridge University Press:
- 25 August 2021, pp. 659-669
- Print publication:
- December 2021
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Background
Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools.
AimsTo examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics.
MethodGenome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts.
ResultsEarlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO.
ConclusionsAAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.
Introducing a psychiatric genetic cohort of schizophrenia patients and controls from Vietnam
- A. Braun, T.V. Nguyen, S. Ripke, P.V. Nguyen, J. Kraft, H.T. Nguyen, T.C. Le, G. Panagiotaropoulou, I.M. Hahne, K. Böge, E. Hahn, T.M.T. Ta
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- Journal:
- European Psychiatry / Volume 64 / Issue S1 / April 2021
- Published online by Cambridge University Press:
- 13 August 2021, pp. S802-S803
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Introduction
Genome-wide association studies (GWAS) have successfully revealed genetic risk variants for schizophrenia (SCZ). However, the vast majority of GWAS largely comprise European samples. As a result, the derived polygenic risk scores (PRS) show decreased predictive power when applied to non-European populations.
ObjectivesA long-term scientific cooperation between the Charité Universitätsmedizin Berlin and the Hanoi Medical University aims to address this limitation by recruiting a large genetic cohort of comprehensively phenotyped schizophrenia patients and controls in Vietnam.
MethodsA pilot study was conducted at the Department of Psychiatry of the Medical University Hanoi in 2017. Data collection encompassed i) genome-wide SNP genotyping of 200 schizophrenia patients and 200 control subjects ii) structured interviews to assess symptom severity (PANSS), iii) clinical parameters (e.g. duration of illness, medication) and demography.
ResultsSCZ-PRS of the pilot sample (N=400) were generated using different training data sets: i) European, ii) East-Asian and iii) mixed GWAS summary statistics from the Psychiatric Genomics Consortium’s latest discovery sample. Most variance explained was observed using a mixed discovery sample (R2liability=0.053, p=3.11*10-8, Pd <0.5), followed by PRS based on the East-Asian summary statistics (R2liability=0.0503, p=6.78*10-8, Pd <1) and the European sample (R2liability=0.0363, p = 4.26*10-6, Pd <0.01).
ConclusionsWith this pilot project we established an efficient recruitment, genotyping and data analysis pipeline. Our results corroborate previous findings indicating that transferability of PRS across populations depends on the ancestral composition of the initial discovery dataset. We therefore aim to expand data collection efforts in the future in order to improve risk prediction across diverse populations.
DisclosureNo significant relationships.
Investigation of convergent and divergent genetic influences underlying schizophrenia and alcohol use disorder
- Emma C. Johnson, Manav Kapoor, Alexander S. Hatoum, Hang Zhou, Renato Polimanti, Frank R. Wendt, Raymond K. Walters, Dongbing Lai, Rachel L. Kember, Sarah Hartz, Jacquelyn L. Meyers, Roseann E. Peterson, Stephan Ripke, Tim B. Bigdeli, Ayman H. Fanous, Carlos N. Pato, Michele T. Pato, Alison M. Goate, Henry R. Kranzler, Michael C. O'Donovan, James T.R. Walters, Joel Gelernter, Howard J. Edenberg, Arpana Agrawal
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- Journal:
- Psychological Medicine / Volume 53 / Issue 4 / March 2023
- Published online by Cambridge University Press:
- 07 July 2021, pp. 1196-1204
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Background
Alcohol use disorder (AUD) and schizophrenia (SCZ) frequently co-occur, and large-scale genome-wide association studies (GWAS) have identified significant genetic correlations between these disorders.
MethodsWe used the largest published GWAS for AUD (total cases = 77 822) and SCZ (total cases = 46 827) to identify genetic variants that influence both disorders (with either the same or opposite direction of effect) and those that are disorder specific.
ResultsWe identified 55 independent genome-wide significant single nucleotide polymorphisms with the same direction of effect on AUD and SCZ, 8 with robust effects in opposite directions, and 98 with disorder-specific effects. We also found evidence for 12 genes whose pleiotropic associations with AUD and SCZ are consistent with mediation via gene expression in the prefrontal cortex. The genetic covariance between AUD and SCZ was concentrated in genomic regions functional in brain tissues (p = 0.001).
ConclusionsOur findings provide further evidence that SCZ shares meaningful genetic overlap with AUD.
Polygenic risk for schizophrenia and schizotypal traits in non-clinical subjects
- Igor Nenadić, Tina Meller, Simon Schmitt, Frederike Stein, Katharina Brosch, Johannes Mosebach, Ulrich Ettinger, Phillip Grant, Susanne Meinert, Nils Opel, Hannah Lemke, Stella Fingas, Katharina Förster, Tim Hahn, Andreas Jansen, Till F. M. Andlauer, Andreas J. Forstner, Stefanie Heilmann-Heimbach, Alisha S. M. Hall, Swapnil Awasthi, Stephan Ripke, Stephanie H. Witt, Marcella Rietschel, Bertram Müller-Myhsok, Markus M. Nöthen, Udo Dannlowski, Axel Krug, Fabian Streit, Tilo Kircher
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- Journal:
- Psychological Medicine / Volume 52 / Issue 6 / April 2022
- Published online by Cambridge University Press:
- 06 August 2020, pp. 1069-1079
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Background
Schizotypy is a putative risk phenotype for psychosis liability, but the overlap of its genetic architecture with schizophrenia is poorly understood.
MethodsWe tested the hypothesis that dimensions of schizotypy (assessed with the SPQ-B) are associated with a polygenic risk score (PRS) for schizophrenia in a sample of 623 psychiatrically healthy, non-clinical subjects from the FOR2107 multi-centre study and a second sample of 1133 blood donors.
ResultsWe did not find correlations of schizophrenia PRS with either overall SPQ or specific dimension scores, nor with adjusted schizotypy scores derived from the SPQ (addressing inter-scale variance). Also, PRS for affective disorders (bipolar disorder and major depression) were not significantly associated with schizotypy.
ConclusionsThis important negative finding demonstrates that despite the hypothesised continuum of schizotypy and schizophrenia, schizotypy might share less genetic risk with schizophrenia than previously assumed (and possibly less compared to psychotic-like experiences).
Temporal delay discounting in acutely ill and weight-recovered patients with anorexia nervosa
- F. Ritschel, J. A. King, D. Geisler, L. Flohr, F. Neidel, I. Boehm, M. Seidel, J. Zwipp, S. Ripke, M. N. Smolka, V. Roessner, S. Ehrlich
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- Psychological Medicine / Volume 45 / Issue 6 / April 2015
- Published online by Cambridge University Press:
- 12 January 2015, pp. 1229-1239
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Background.
Patients with anorexia nervosa (AN) are characterized by a very low body weight but readily give up immediate rewards (food) for long-term goals (slim figure), which might indicate an unusual level of self-control. This everyday clinical observation may be quantifiable in the framework of the anticipation-discounting dilemma.
Method.Using a cross-sectional design, this study compared the capacity to delay reward in 34 patients suffering from acute AN (acAN), 33 weight-recovered AN patients (recAN) and 54 healthy controls. We also used a longitudinal study to reassess 21 acAN patients after short-term weight restoration. A validated intertemporal choice task and a hyperbolic model were used to estimate temporal discounting rates.
Results.Confirming the validity of the task used, decreased delay discounting was associated with age and low self-reported impulsivity. However, no group differences in key measures of temporal discounting of monetary rewards were found.
Conclusions.Increased cognitive control, which has been suggested as a key characteristic of AN, does not seem to extend the capacity to wait for delayed monetary rewards. Differences between our study and the only previous study reporting decreased delay discounting in adult AN patients may be explained by the different age range and chronicity of acute patients, but the fact that weight recovery was not associated with changes in discount rates suggests that discounting behavior is not a trait marker in AN. Future studies using paradigms with disorder-specific stimuli may help to clarify the role of delay discounting in AN.
Schizophrenia genetic variants are not associated with intelligence
- A. F. Terwisscha van Scheltinga, S. C. Bakker, N. E. M. van Haren, E. M. Derks, J. E. Buizer-Voskamp, W. Cahn, S. Ripke, R. A. Ophoff, R. S. Kahn
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- Journal:
- Psychological Medicine / Volume 43 / Issue 12 / December 2013
- Published online by Cambridge University Press:
- 15 February 2013, pp. 2563-2570
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Background
Schizophrenia is associated with lower pre-morbid intelligence (IQ) in addition to (pre-morbid) cognitive decline. Both schizophrenia and IQ are highly heritable traits. Therefore, we hypothesized that genetic variants associated with schizophrenia, including copy number variants (CNVs) and a polygenic schizophrenia (risk) score (PSS), may influence intelligence.
MethodIQ was estimated with the Wechsler Adult Intelligence Scale (WAIS). CNVs were determined from single nucleotide polymorphism (SNP) data using the QuantiSNP and PennCNV algorithms. For the PSS, odds ratios for genome-wide SNP data were calculated in a sample collected by the Psychiatric Genome-Wide Association Study (GWAS) Consortium (8690 schizophrenia patients and 11 831 controls). These were used to calculate individual PSSs in our independent sample of 350 schizophrenia patients and 322 healthy controls.
ResultsAlthough significantly more genes were disrupted by deletions in schizophrenia patients compared to controls (p = 0.009), there was no effect of CNV measures on IQ. The PSS was associated with disease status (R2 = 0.055, p = 2.1 × 10−7) and with IQ in the entire sample (R2 = 0.018, p = 0.0008) but the effect on IQ disappeared after correction for disease status.
ConclusionsOur data suggest that rare and common schizophrenia-associated variants do not explain the variation in IQ in healthy subjects or in schizophrenia patients. Thus, reductions in IQ in schizophrenia patients may be secondary to other processes related to schizophrenia risk.