Marta de Castro-Catala1, Elionora Peña1, Thomas R Kwapil2, Sergi Papiol3, Tamara Sheinbaum4, Paula Cristóbal-Narváez4, Sergi Ballespí4, Neus Barrantes-Vidal5, Araceli Rosa6. 1. Secció de Zoologia i Antropologia Biològica, Departament de Biologia Evolutiva, Ecologia i Ciències Ambientals, Universitat de Barcelona (UB), Avinguda Diagonal 643, 08028 Barcelona, Spain; Institut de Biomedicina de la Universitat de Barcelona (IBUB), Barcelona, Spain. 2. Department of Psychology, University of North Carolina at Greensboro, Greensboro, NC 27402-6170, United States; Department of Psychology, University of Illinois at Champaign-Urbana, Champaign, IL 61820, United States. 3. Department of Psychiatry and Psychotherapy, Ludwig Maximilian University Munich, Nussbaumstrasse 7, 80336 Munich, Germany; Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital, LMU Munich, Nussbaumstrasse 7, 80336 Munich, Germany; Centre for Biomedical Research Network on Mental Health (CIBERSAM), Instituto Carlos III, Madrid, Spain. 4. Departament de Psicologia Clínica i de la Salut, Facultat de Psicologia, Universitat Autònoma de Barcelona (UAB), 08193 Bellaterra, Barcelona, Spain. 5. Department of Psychology, University of North Carolina at Greensboro, Greensboro, NC 27402-6170, United States; Centre for Biomedical Research Network on Mental Health (CIBERSAM), Instituto Carlos III, Madrid, Spain; Departament de Psicologia Clínica i de la Salut, Facultat de Psicologia, Universitat Autònoma de Barcelona (UAB), 08193 Bellaterra, Barcelona, Spain; Sant Pere Claver-Fundació Sanitària Carrer Vila i Vilà 16, 08004 Barcelona, Spain. 6. Secció de Zoologia i Antropologia Biològica, Departament de Biologia Evolutiva, Ecologia i Ciències Ambientals, Universitat de Barcelona (UB), Avinguda Diagonal 643, 08028 Barcelona, Spain; Institut de Biomedicina de la Universitat de Barcelona (IBUB), Barcelona, Spain; Centre for Biomedical Research Network on Mental Health (CIBERSAM), Instituto Carlos III, Madrid, Spain. Electronic address: araceli.rosa@ub.edu.
Abstract
BACKGROUND: Childhood trauma has been associated with a heightened risk for presenting clinical and non-clinical psychopathology in adulthood. Genes related with the stress response, such as the FK506 binding protein 51 (FKBP5), are plausible candidates moderating the effects of childhood trauma on the emergence of such symptoms later on. The present study aimed to explore the moderating role of FKBP5 genetic variability on the association of different types of childhood trauma with subclinical psychosis, depression and anxiety in a non-clinical sample. METHODS: Schizotypy, psychotic-like experiences, depression and anxiety symptoms and childhood trauma were assessed in 808 young adults. Two FKBP5 haplotypic blocks were detected: block 1 (rs3800373 - rs9296158 - rs1360780) and block 2 (rs9470080 - rs4713916). Subjects were classified in two groups according to whether they carried or not the risk haplotype previously described in the literature (block 1: CAT and block 2: TA). Linear regression analyses were used to study (i) the main effects of childhood trauma and FKBP5 haplotype blocks and (ii) their interaction effects on the mentioned forms of psychopathology. RESULTS: All childhood trauma scales, except sexual abuse, were associated with schizotypy, psychotic-like experiences, depression and anxiety symptoms. None of the analysed symptoms was associated with the main effects of FKBP5 genetic variability. However an interaction effect between block 1 and physical abuse was observed on anxiety, with lower scores in CAT carriers. This effect was driven by SNP 1 and 2. Moreover, an interaction effect between block 2 and physical abuse was identified on the variables tapping depressive and anxiety symptoms. Specifically, non-TA carrier subjects who were exposed to physical abuse were found to be at higher risk for depressive and anxiety symptoms. These effects were driven by SNP 5. No interaction effect was observed for the other variables. CONCLUSIONS: Our data suggest that exposure to childhood physical abuse may increase the risk for sub-clinical depressive and anxiety symptoms depending on FKBP5 genetic variability. Further research is needed to better elucidate the role of FKBP5 on mental health in clinical and non-clinical cohorts.
BACKGROUND:Childhood trauma has been associated with a heightened risk for presenting clinical and non-clinical psychopathology in adulthood. Genes related with the stress response, such as the FK506 binding protein 51 (FKBP5), are plausible candidates moderating the effects of childhood trauma on the emergence of such symptoms later on. The present study aimed to explore the moderating role of FKBP5 genetic variability on the association of different types of childhood trauma with subclinical psychosis, depression and anxiety in a non-clinical sample. METHODS: Schizotypy, psychotic-like experiences, depression and anxiety symptoms and childhood trauma were assessed in 808 young adults. Two FKBP5 haplotypic blocks were detected: block 1 (rs3800373 - rs9296158 - rs1360780) and block 2 (rs9470080 - rs4713916). Subjects were classified in two groups according to whether they carried or not the risk haplotype previously described in the literature (block 1: CAT and block 2: TA). Linear regression analyses were used to study (i) the main effects of childhood trauma and FKBP5 haplotype blocks and (ii) their interaction effects on the mentioned forms of psychopathology. RESULTS: All childhood trauma scales, except sexual abuse, were associated with schizotypy, psychotic-like experiences, depression and anxiety symptoms. None of the analysed symptoms was associated with the main effects of FKBP5 genetic variability. However an interaction effect between block 1 and physical abuse was observed on anxiety, with lower scores in CAT carriers. This effect was driven by SNP 1 and 2. Moreover, an interaction effect between block 2 and physical abuse was identified on the variables tapping depressive and anxiety symptoms. Specifically, non-TA carrier subjects who were exposed to physical abuse were found to be at higher risk for depressive and anxiety symptoms. These effects were driven by SNP 5. No interaction effect was observed for the other variables. CONCLUSIONS: Our data suggest that exposure to childhood physical abuse may increase the risk for sub-clinical depressive and anxiety symptoms depending on FKBP5 genetic variability. Further research is needed to better elucidate the role of FKBP5 on mental health in clinical and non-clinical cohorts.
Authors: Filip Stramecki; Dorota Frydecka; Łukasz Gawęda; Katarzyna Prochwicz; Joanna Kłosowska; Jerzy Samochowiec; Krzysztof Szczygieł; Edyta Pawlak; Elżbieta Szmida; Paweł Skiba; Andrzej Cechnicki; Błażej Misiak Journal: Brain Sci Date: 2021-04-28
Authors: Juan P Sanabria-Mazo; Carlos G Forero; Paula Cristobal-Narváez; Carlos Suso-Ribera; Azucena García-Palacios; Ariadna Colomer-Carbonell; Adrián Pérez-Aranda; Laura Andrés-Rodríguez; Lance M McCracken; Francesco D'Amico; Pere Estivill-Rodríguez; Bernat Carreras-Marcos; Antonio Montes-Pérez; Olga Comps-Vicente; Montserrat Esteve; Mar Grasa; Araceli Rosa; Antonio I Cuesta-Vargas; Michael Maes; Xavier Borràs; Silvia Edo; Antoni Sanz; Albert Feliu-Soler; Juan R Castaño-Asins; Juan V Luciano Journal: BMJ Open Date: 2020-07-23 Impact factor: 2.692
Authors: José Gulfo; Joana Pérez de San Román; Angelo Ledda; Felix Junyent; María J Ramírez; Francisco J Gil-Bea; Montserrat Esteve; Mar Grasa Journal: PLoS One Date: 2021-02-16 Impact factor: 3.240