Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Feb 17:5:14.
doi: 10.3389/fendo.2014.00014. eCollection 2014.

Gene-environment interactions and intermediate phenotypes: early trauma and depression

Affiliations
Review

Gene-environment interactions and intermediate phenotypes: early trauma and depression

Orla P Hornung et al. Front Endocrinol (Lausanne). .

Abstract

This review focuses on current research developments in the study of gene by early life stress (ELS) interactions and depression. ELS refers to aversive experiences during childhood and adolescence such as sexual, physical or emotional abuse, emotional or physical neglect as well as parental loss. Previous research has focused on investigating and characterizing the specific role of ELS within the pathogenesis of depression and linking these findings to neurobiological changes of the brain, especially the stress response system. The latest findings highlight the role of genetic factors that increase vulnerability or, likewise, promote resilience to depression after childhood trauma. Considering intermediate phenotypes has further increased our understanding of the complex relationship between early trauma and depression. Recent findings with regard to epigenetic changes resulting from adverse environmental events during childhood promote current endeavors to identify specific target areas for prevention and treatment schemes regarding the long-term impact of ELS. Taken together, the latest research findings have underscored the essential role of genotypes and epigenetic processes within the development of depression after childhood trauma, thereby building the basis for future research and clinical interventions.

Keywords: HPA axis; depression; development; maltreatment; polymorphisms; stress.

PubMed Disclaimer

References

    1. Nestler EJ, Barrot M, DiLeone RJ, Eisch AJ, Gold SJ, Monteggia LM. Neurobiology of depression. Neuron (2002) 34(1):13–2510.1016/S0896-6273(02)00653-0 - DOI - PubMed
    1. Davidson RJ, McEwen BS. Social influences on neuroplasticity: stress and interventions to promote well-being. Nat Neurosci (2012) 15(5):689–9510.1038/nn.3093 - DOI - PMC - PubMed
    1. Heim C, Binder EB. Current research trends in early life stress and depression: review of human studies on sensitive periods, gene-environment interactions, and epigenetics. Exp Neurol (2011) 233(1):102–1110.1016/j.expneurol.2011.10.032 - DOI - PubMed
    1. Meyer-Lindenberg A, Tost H. Neural mechanisms of social risk for psychiatric disorders. Nat Neurosci (2012) 15(5):663–810.1038/nn.3083 - DOI - PubMed
    1. Pechtel P, Pizzagalli DA. Effects of early life stress on cognitive and affective function: an integrated review of human literature. Psychopharmacology (Berl) (2011) 214(1):55–7010.1007/s00213-010-2009-2 - DOI - PMC - PubMed

LinkOut - more resources