Contribution in an anthology

Appeared in: Epigenetics and Neuroendocrinology: Clinical Focus on Psychiatry, Volume 2

Editor list: Spengler, Dietmar; Binder, Elisabeth

Publication year: 2016

Pages: 197-207

ISBN: 978-3-319-29900-6

eISBN: 978-3-319-29901-3

DOI Link: https://doi.org/10.1007/978-3-319-29901-3_9

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.

Harvard Citation style: Dammann, R. and Dammann, G. (2016) Epigenetic Modifications in Borderline Personality Disorder, in Spengler, D. and Binder, E. (eds.) Epigenetics and Neuroendocrinology: Clinical Focus on Psychiatry, Volume 2. Cham: Springer, pp. 197-207. https://doi.org/10.1007/978-3-319-29901-3_9

APA Citation style: Dammann, R., & Dammann, G. (2016). Epigenetic Modifications in Borderline Personality Disorder. In Spengler, D., & Binder, E. (Eds.), Epigenetics and Neuroendocrinology: Clinical Focus on Psychiatry, Volume 2 (pp. 197-207). Springer. https://doi.org/10.1007/978-3-319-29901-3_9