What DNA methylation modifications and/or genetic variations interact with childhood maltreatment in the development...

Child maltreatment predicts a significant risk factor for depression. The relationship between child maltreatment and depression has been shown to vary as a function of genetic factors. There have been very few systematic reviews conducted to date to synthesize what DNA methylations and/ or genetic variations interact with childhood maltreatment in the course of depression. This systematic review aimed to provide an overview of DNA methylation modifications with/without genetic variations associated with childhood maltreatment in depression.

Computerized and manual search on six databases (EMBASE, HealthStar, PsychoInfo, Medline, PubMed and Cochrane Library) and grey literature up to June 30th 2018 were conducted. Studies were critically evaluated for their eligibility and study quality.

The initial search resulted in 196 articles. Five articles met the eligibility criteria being included in this review. All the selected studies were from the United States and published within the last five years. Changes in ID3, TPPP, GRIN1, and OXTR DNA methylation sites were found to be involved in the childhood maltreatment-depression relationship.

The number of eligible articles included in this review was small. Selected articles had small sample sizes. A high degree of heterogeneity was found. It is difficult to conclude what the roles of DNA methylation modifications are in the relationship between maltreatment and depression. Population stratification has not been extensively studied so far and should be considered in the further research.

This review synthesizes an overview of the interaction between childhood maltreatment, DNA methylation modifications and genetic variations in depression. Findings of this review highlight an urgent need for genetic and epigenetic research in the area of childhood maltreatment and depression. Future etiological explorations should target on the above identified sites.