Epigenetic Modifications in Borderline Personality Disorder

Abstract

Borderline personality disorder (BPD) is a complex psychic disease with an increased importance in the last years. While the diagnosis and therapy are well established, little is known on the pathogenesis of BPD. Epigenetic alterations are a hallmark for abnormal gene expression and could be involved in the etiology of BPD. These epigenetic changes are mainly classified into altered histone modifications and DNA methylation. Here, we summarize recent findings on epigenetic alterations in BPD. Significant aberrant DNA methylation of serotonin receptor 2A (HTR2A), monoamine oxidase A and B (MAOA and MAOB), glucocorticoid receptor (GR/NR3C1), brain derived neurotrophic factor (BDNF), amyloid beta precursor protein-binding family A member 2 and 3 (APBA2 and APBA3), KCNQ1, MCF2, and ninjurin 2 (NINJ2) has been reported. DNA methylation changes range between 1.1-and 1.5-fold increased methylation in the blood of BPD subjects. Especially, GR/NR3C1 methylation was positively associated with childhood maltreatment and clinical severity in BPD. These data may provide new insights into epigenetic mechanisms underlying the pathogenesis of borderline personality disorder.