Interactions Between Variation in Candidate Genes and Environmental Factors in the Etiology of Schizophrenia and Bipolar Disorder: a Systematic Review View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-08-18

AUTHORS

Błażej Misiak, Filip Stramecki, Łukasz Gawęda, Katarzyna Prochwicz, Maria M. Sąsiadek, Ahmed A. Moustafa, Dorota Frydecka

ABSTRACT

Schizophrenia and bipolar disorder (BD) are complex and multidimensional disorders with high heritability rates. The contribution of genetic factors to the etiology of these disorders is increasingly being recognized as the action of multiple risk variants with small effect sizes, which might explain only a minor part of susceptibility. On the other site, numerous environmental factors have been found to play an important role in their causality. Therefore, in recent years, several studies focused on gene × environment interactions that are believed to bridge the gap between genetic underpinnings and environmental insults. In this article, we performed a systematic review of studies investigating gene × environment interactions in BD and schizophrenia spectrum phenotypes. In the majority of studies from this field, interacting effects of variation in genes encoding catechol-O-methyltransferase (COMT), brain-derived neurotrophic factor (BDNF), and FK506-binding protein 5 (FKBP5) have been explored. Almost consistently, these studies revealed that polymorphisms in COMT, BDNF, and FKBP5 genes might interact with early life stress and cannabis abuse or dependence, influencing various outcomes of schizophrenia spectrum disorders and BD. Other interactions still require further replication in larger clinical and non-clinical samples. In addition, future studies should address the direction of causality and potential mechanisms of the relationship between gene × environment interactions and various categories of outcomes in schizophrenia and BD. More... »

PAGES

5075-5100

References to SciGraph publications

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  • 2012-12-19. Design and analysis issues in gene and environment studies in ENVIRONMENTAL HEALTH
  • 2009-07-25. Adolescent Cannabis Use, Psychosis and Catechol-O-Methyltransferase Genotype in African Americans and Caucasians in PSYCHIATRIC QUARTERLY
  • 2014-10-05. COMT and STH polymorphisms interaction on cognition in schizophrenia in NEUROLOGICAL SCIENCES
  • 2013-08-11. Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs in NATURE GENETICS
  • 2011-09-18. Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near ODZ4 in NATURE GENETICS
  • Identifiers

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    http://scigraph.springernature.com/pub.10.1007/s12035-017-0708-y

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    DIMENSIONS

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    33 schema:description Schizophrenia and bipolar disorder (BD) are complex and multidimensional disorders with high heritability rates. The contribution of genetic factors to the etiology of these disorders is increasingly being recognized as the action of multiple risk variants with small effect sizes, which might explain only a minor part of susceptibility. On the other site, numerous environmental factors have been found to play an important role in their causality. Therefore, in recent years, several studies focused on gene × environment interactions that are believed to bridge the gap between genetic underpinnings and environmental insults. In this article, we performed a systematic review of studies investigating gene × environment interactions in BD and schizophrenia spectrum phenotypes. In the majority of studies from this field, interacting effects of variation in genes encoding catechol-O-methyltransferase (COMT), brain-derived neurotrophic factor (BDNF), and FK506-binding protein 5 (FKBP5) have been explored. Almost consistently, these studies revealed that polymorphisms in COMT, BDNF, and FKBP5 genes might interact with early life stress and cannabis abuse or dependence, influencing various outcomes of schizophrenia spectrum disorders and BD. Other interactions still require further replication in larger clinical and non-clinical samples. In addition, future studies should address the direction of causality and potential mechanisms of the relationship between gene × environment interactions and various categories of outcomes in schizophrenia and BD.
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