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Epigenetics: A missing link between early life stress and depression
Mario F Juruena1, Romayne Gadelrab2, Anthony J Cleare1
1Centre for Affective Disorders, Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, Denmark Hill, London SE5 8AF, UK; South London and Maudsley NHS Foundation Trust (SLaM), UK.
Progress in Neuro-Psychopharmacology & Biological Psychiatry
|December 31, 2020
Summary
Early life stress is linked to persistent depression, but mechanisms are unclear. Epigenetic factors, like DNA methylation, offer new insights into depression development and potential treatments.
Area of Science:
- Neuroscience
- Psychiatry
- Genetics
Background:
- Early life stress is associated with depression, particularly treatment-resistant forms.
- The precise molecular mechanisms linking early stress to depression remain largely unknown.
- Psychiatric disorders have complex genetic underpinnings, involving interactions between numerous low-effect variants.
Purpose of the Study:
- To explore the interplay between epigenetics, the hypothalamic-pituitary-adrenal (HPA) axis, early life stress, and depression.
- To provide an overview of current understanding regarding these complex interactions.
Main Methods:
- Review of molecular and epigenetic studies.
- Focus on DNA methylation, histone modifications, and non-coding RNA regulation.
- Examination of the HPA axis in the context of stress and depression.
Main Results:
- Epigenetic mechanisms, including DNA methylation and histone modifications, play a crucial role in psychiatric disorders.
- Gene-environment interactions are fundamental, with epigenetics mediating these effects.
- The HPA axis is a key pathway influenced by early life stress, impacting depression.
Conclusions:
- Advances in understanding epigenetics in early life stress and depression illuminate genetic influences on psychopathology.
- This knowledge may lead to novel therapeutic targets for depression.
- Epigenetic modifications offer a bridge between environmental exposures and genetic predisposition in depression.
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