An integrative review of methylation at the serotonin transporter gene and its dialogue with environmental risk factors, psychopathology and 5-HTTLPR
•Exposure to both early and recent stress is associated with SLC6A4 hypermethylation.•SLC6A4 hypermethylation is found in subjects suffering from psychiatric disorders.•s carriers exposed to early stress are at higher odds of developing psychopathology.•Several confounding factors have to be address...
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| Published in | Neuroscience and biobehavioral reviews Vol. 72; pp. 190 - 209 |
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| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Ltd
01.01.2017
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0149-7634 1873-7528 1873-7528 |
| DOI | 10.1016/j.neubiorev.2016.11.011 |
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| Abstract | •Exposure to both early and recent stress is associated with SLC6A4 hypermethylation.•SLC6A4 hypermethylation is found in subjects suffering from psychiatric disorders.•s carriers exposed to early stress are at higher odds of developing psychopathology.•Several confounding factors have to be addressed in further analyses.
Gene—environment (G×E) interactions have largely been regarded as the root of many complex disorders, including several psychiatric disorders. In this regard, it has been hypothesized that epigenetic mechanisms may be the main mediators of such interactions. Of particular interest is the previously described interaction between psychosocial stress and genetic variability of the serotonin transporter gene (SLC6A4) in its polymorphic region 5-HTTLPR. Here we review the literature concerning SLC6A4 methylation in association with environmental, clinical or genetic variables. While SLC6A4 hypermethylation has typically been described to be independently associated with both early life stress and depressive disorders, only a few papers address whether methylation could mediate the interaction between stress and 5-HTTLPR in predicting psychopathological risk. Nevertheless, research preliminarily indicates a methylation-driven increased vulnerability of carriers of the short allele of 5-HTTLPR to psychiatric disorders when exposed to early stress or soon after exposure to stress. |
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| AbstractList | Gene-environment (G×E) interactions have largely been regarded as the root of many complex disorders, including several psychiatric disorders. In this regard, it has been hypothesized that epigenetic mechanisms may be the main mediators of such interactions. Of particular interest is the previously described interaction between psychosocial stress and genetic variability of the serotonin transporter gene (SLC6A4) in its polymorphic region 5-HTTLPR. Here we review the literature concerning SLC6A4 methylation in association with environmental, clinical or genetic variables. While SLC6A4 hypermethylation has typically been described to be independently associated with both early life stress and depressive disorders, only a few papers address whether methylation could mediate the interaction between stress and 5-HTTLPR in predicting psychopathological risk. Nevertheless, research preliminarily indicates a methylation-driven increased vulnerability of carriers of the short allele of 5-HTTLPR to psychiatric disorders when exposed to early stress or soon after exposure to stress.Gene-environment (G×E) interactions have largely been regarded as the root of many complex disorders, including several psychiatric disorders. In this regard, it has been hypothesized that epigenetic mechanisms may be the main mediators of such interactions. Of particular interest is the previously described interaction between psychosocial stress and genetic variability of the serotonin transporter gene (SLC6A4) in its polymorphic region 5-HTTLPR. Here we review the literature concerning SLC6A4 methylation in association with environmental, clinical or genetic variables. While SLC6A4 hypermethylation has typically been described to be independently associated with both early life stress and depressive disorders, only a few papers address whether methylation could mediate the interaction between stress and 5-HTTLPR in predicting psychopathological risk. Nevertheless, research preliminarily indicates a methylation-driven increased vulnerability of carriers of the short allele of 5-HTTLPR to psychiatric disorders when exposed to early stress or soon after exposure to stress. Gene-environment (G×E) interactions have largely been regarded as the root of many complex disorders, including several psychiatric disorders. In this regard, it has been hypothesized that epigenetic mechanisms may be the main mediators of such interactions. Of particular interest is the previously described interaction between psychosocial stress and genetic variability of the serotonin transporter gene (SLC6A4) in its polymorphic region 5-HTTLPR. Here we review the literature concerning SLC6A4 methylation in association with environmental, clinical or genetic variables. While SLC6A4 hypermethylation has typically been described to be independently associated with both early life stress and depressive disorders, only a few papers address whether methylation could mediate the interaction between stress and 5-HTTLPR in predicting psychopathological risk. Nevertheless, research preliminarily indicates a methylation-driven increased vulnerability of carriers of the short allele of 5-HTTLPR to psychiatric disorders when exposed to early stress or soon after exposure to stress. •Exposure to both early and recent stress is associated with SLC6A4 hypermethylation.•SLC6A4 hypermethylation is found in subjects suffering from psychiatric disorders.•s carriers exposed to early stress are at higher odds of developing psychopathology.•Several confounding factors have to be addressed in further analyses. Gene—environment (G×E) interactions have largely been regarded as the root of many complex disorders, including several psychiatric disorders. In this regard, it has been hypothesized that epigenetic mechanisms may be the main mediators of such interactions. Of particular interest is the previously described interaction between psychosocial stress and genetic variability of the serotonin transporter gene (SLC6A4) in its polymorphic region 5-HTTLPR. Here we review the literature concerning SLC6A4 methylation in association with environmental, clinical or genetic variables. While SLC6A4 hypermethylation has typically been described to be independently associated with both early life stress and depressive disorders, only a few papers address whether methylation could mediate the interaction between stress and 5-HTTLPR in predicting psychopathological risk. Nevertheless, research preliminarily indicates a methylation-driven increased vulnerability of carriers of the short allele of 5-HTTLPR to psychiatric disorders when exposed to early stress or soon after exposure to stress. |
| Author | Palma-Gudiel, H. Fañanás, L. |
| Author_xml | – sequence: 1 givenname: H. surname: Palma-Gudiel fullname: Palma-Gudiel, H. organization: Department of Evolutionary Biology, Ecology and Environmental Sciences, Faculty of Biology, University of Barcelona, Spain – sequence: 2 givenname: L. surname: Fañanás fullname: Fañanás, L. email: lfananas@ub.edu organization: Department of Evolutionary Biology, Ecology and Environmental Sciences, Faculty of Biology, University of Barcelona, Spain |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27880876$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | 5-HTTLPR DNA Methylation G × E interaction Genotype Humans Risk Factors Serotonin Plasma Membrane Transport Proteins - metabolism SLC6A4 gene Stress, Psychological |
| Title | An integrative review of methylation at the serotonin transporter gene and its dialogue with environmental risk factors, psychopathology and 5-HTTLPR |
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