scholarly journals TH68. METABOLIC POLYGENIC RISK SCORES EFFECT ON ANTIPSYCHOTIC-INDUCED METABOLIC DYSREGULATION: A LONGITUDINAL STUDY IN A FIRST EPISODE PSYCHOSIS COHORT

2021 ◽  
Vol 51 ◽  
pp. e230-e231
Author(s):  
Patricia Gassó ◽  
Alex G. Segura ◽  
Albert Martínez-Pinteño ◽  
Natalia Rodríguez ◽  
Bernardo Miquel ◽  
...  
2019 ◽  
Author(s):  
M Montagnese ◽  
F Knolle ◽  
J Haarsma ◽  
JD Griffin ◽  
A Richards ◽  
...  

AbstractBackgroundSchizophrenia is a complex disorder in which the causal relations between risk genes and observed clinical symptoms are not well understood and the explanatory gap is too wide to be clarified without considering an intermediary level. Thus, we aimed to test the hypothesis of a pathway from molecular polygenic influence to clinical presentation occurring via deficits in reinforcement learning.MethodsWe administered a reinforcement learning task (Go/NoGo) that measures reinforcement learning and the effect of Pavlovian bias on decision making. We modelled the behavioural data with a hierarchical Bayesian approach (hBayesDM) to decompose task performance into its underlying learning mechanisms. Study 1 included controls (n= 29, F|M=0.81), At Risk Mental State for psychosis (ARMS, n= 23, F|M=0.35) and FEP (First-episode psychosis, n= 26, F|M=0.18). Study 2 included healthy adolescents (n= 735, F|M= 1.06), 390 of whom had their polygenic risk scores for schizophrenia (PRSs) calculated.ResultsPatients with FEP showed significant impairments in overriding Pavlovian conflict, a lower learning rate and a lower sensitivity to both reward and punishment. Less widespread deficits were observed in ARMS. PRSs did not significantly predict performance on the task in the general population, which only partially correlated with measures of psychopathology.ConclusionsReinforcement learning deficits are observed in first episode psychosis and, to some extent, in those at clinical risk for psychosis, and were not predicted by molecular genetic risk for schizophrenia in healthy individuals. The study does not support the role of reinforcement learning as an intermediate phenotype in psychosis.


2011 ◽  
Vol 126 (1-3) ◽  
pp. 77-80 ◽  
Author(s):  
Javier Peña ◽  
Natalia Ojeda ◽  
Rafael Segarra ◽  
Jose Ignacio Eguiluz ◽  
Jon García ◽  
...  

2019 ◽  
Vol 50 (1) ◽  
pp. 173-176
Author(s):  
Diego Quattrone ◽  
Alex Richards ◽  
Ulrich Reininghaus ◽  
Evangelos Vassos ◽  
Michael O'Donovan ◽  
...  

2020 ◽  
pp. 1-11 ◽  
Author(s):  
Giada Tripoli ◽  
Diego Quattrone ◽  
Laura Ferraro ◽  
Charlotte Gayer-Anderson ◽  
Victoria Rodriguez ◽  
...  

Abstract Background The ‘jumping to conclusions’ (JTC) bias is associated with both psychosis and general cognition but their relationship is unclear. In this study, we set out to clarify the relationship between the JTC bias, IQ, psychosis and polygenic liability to schizophrenia and IQ. Methods A total of 817 first episode psychosis patients and 1294 population-based controls completed assessments of general intelligence (IQ), and JTC, and provided blood or saliva samples from which we extracted DNA and computed polygenic risk scores for IQ and schizophrenia. Results The estimated proportion of the total effect of case/control differences on JTC mediated by IQ was 79%. Schizophrenia polygenic risk score was non-significantly associated with a higher number of beads drawn (B = 0.47, 95% CI −0.21 to 1.16, p = 0.17); whereas IQ PRS (B = 0.51, 95% CI 0.25–0.76, p < 0.001) significantly predicted the number of beads drawn, and was thus associated with reduced JTC bias. The JTC was more strongly associated with the higher level of psychotic-like experiences (PLEs) in controls, including after controlling for IQ (B = −1.7, 95% CI −2.8 to −0.5, p = 0.006), but did not relate to delusions in patients. Conclusions Our findings suggest that the JTC reasoning bias in psychosis might not be a specific cognitive deficit but rather a manifestation or consequence, of general cognitive impairment. Whereas, in the general population, the JTC bias is related to PLEs, independent of IQ. The work has the potential to inform interventions targeting cognitive biases in early psychosis.


2019 ◽  
Vol 10 ◽  
Author(s):  
Xiao Wei Tan ◽  
Shazana Shahwan ◽  
Pratika Satghare ◽  
Boon Yiang Chua ◽  
Swapna Verma ◽  
...  

2019 ◽  
Vol 14 (4) ◽  
pp. 507-511 ◽  
Author(s):  
Carlo Maj ◽  
Sarah Tosato ◽  
Roberta Zanardini ◽  
Antonio Lasalvia ◽  
Angela Favaro ◽  
...  

2013 ◽  
Vol 4 ◽  
Author(s):  
Rosa Ayesa-Arriola ◽  
Roberto Roiz-Santiáñez ◽  
Rocío Pérez-Iglesias ◽  
Adele Ferro ◽  
Jesús Sainz ◽  
...  

2019 ◽  
Author(s):  
Diego Quattrone ◽  
Ulrich Reininghaus ◽  
Alex L. Richards ◽  
Giada Tripoli ◽  
Laura Ferraro ◽  
...  

AbstractBackgroundDiagnostic categories within the psychosis spectrum are widely used in clinical practice, however psychosis may occur on a continuum. Therefore, we explored whether the continuous distribution of psychotic symptoms across categories is a function of genetic as well as environmental risk factors, such as polygenic risk scores (PRSs) and cannabis use.MethodsAs part of the EU-GEI study, we genotyped first episode psychosis patients (FEP) and population controls, for whom transdiagnostic dimensions of psychotic symptoms or experiences were generated using item response bi-factor modelling. Linear regression was used, separately in patients and controls, to test the associations between these dimensions and schizophrenia (SZ) PRSs, as well as the combined effect of SZ-PRS and cannabis use on the positive symptom/experience dimensions.ResultsSZ-PRS was associated with negative (B=0.18; 95%CI 0.03 to 0.34) and positive (B=0.19; 95%CI 0.03 to 0.36) symptom dimensions in 617 FEP, and with all the psychotic experience dimensions in 979 controls. The putative effect of SZ-PRS on either symptom or experience dimensions was of a small magnitude. Cannabis use was additionally associated with the positive dimensions both in FEP (B=0.31; 95%CI 0.11 to 0.52) and in controls (B=0.26; 95%CI 0.06 to 0.46), independently from SZ-PRS.ConclusionsWe report two validators to the latent dimensional structure of psychosis. SZ risk variants and cannabis use independently map onto specific dimensions, contributing to variation across the psychosis continuum. Findings support the hypothesis that psychotic experiences have similar biological substrates as clinical disorders.


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