Understanding the Molecular Biology in the Pathogenesis of Depression.
- Author:
Jung Goo LEE
1
;
Mi Kyoung SEO
;
Sung Woo PARK
;
Jun Hyung BAEK
;
Young Hoon KIM
Author Information
1. Department of Psychiatry, Haeundae Paik Hospital, College of Medicine, Inje University, Busan, Korea. iybihwc@chol.com
- Publication Type:Review
- Keywords:
Depression;
Pathophysiology;
Monoamine hypothesis;
Neural plasticity;
mTOR signaling
- MeSH:
Biology;
Depression;
Epigenomics;
Humans;
Molecular Biology;
Plastics;
Prevalence;
Sirolimus;
Suicide
- From:Korean Journal of Psychopharmacology
2012;23(4):147-154
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Depression is a common psychiatric illness with a high lifetime prevalence in the general population. Serious problem, such as suicide is commonly occurring in the patients with depression. Till now, the monoamine hypothesis has been the most popular theory of pathogenesis for depression. However, the more specific pathophysiology of depression and cellular molecular mechanism underlying action of commercial antidepressant has not been clearly defined. Several recent studies demonstrated that neural plasticity, epigenetic and mammalian target of rapamycin signaling are promising answers to the pathophysiology of depression. In this article, current understanding of biology and molecular mechanisms of depression and new research on the pathophysiology of depression will be discussed.
