scholarly journals Major Depressive Disorder: Advances in Neuroscience Research and Translational Applications

Author(s):  
Zezhi Li ◽  
Meihua Ruan ◽  
Jun Chen ◽  
Yiru Fang

AbstractMajor depressive disorder (MDD), also referred to as depression, is one of the most common psychiatric disorders with a high economic burden. The etiology of depression is still not clear, but it is generally believed that MDD is a multifactorial disease caused by the interaction of social, psychological, and biological aspects. Therefore, there is no exact pathological theory that can independently explain its pathogenesis, involving genetics, neurobiology, and neuroimaging. At present, there are many treatment measures for patients with depression, including drug therapy, psychotherapy, and neuromodulation technology. In recent years, great progress has been made in the development of new antidepressants, some of which have been applied in the clinic. This article mainly reviews the research progress, pathogenesis, and treatment of MDD.

2018 ◽  
Vol 8 (2) ◽  
pp. 35-39
Author(s):  
Chidiebere Michael Iro ◽  
Rami Hamati

Major depressive disorder (MDD) is a multifaceted, debilitating condition affecting over 300 million people worldwide. It contributes significantly to social, psychological and economic burdens on individuals and on society at large. Currently, the most widely prescribed antidepressant medications are selective serotonin reuptake inhibitors (SSRIs), which act by blocking serotonin (5-HT) reuptake into presynaptic neurons, thereby increasing the extracellular 5-HT concentration in the brain. However, response to SSRIs and other psychotropic medications used to treat depression is highly variable, with only about one third of patients responding to treatment with an SSRI. This may reflect, at least in part, the genetic heterogeneity of depressed individuals. Studies investigating the genetic components of depression aim to improve treatment outcomes and possibly pave the way for personalized medicine in which the first medication prescribed is the one most likely to result in remission. This review presents the results of several studies on two 5-HT related genes: SLC6A4 and HTR2A, which encode for the serotonin transporter and the serotonin-2A receptor, respectively. Extensive studies have demonstrated that possessing two copies of the long allele (L/L) of the SLC6A4 gene can predict better responses to the SSRI Escitalopram. However, this finding was significant only in the Caucasian population. In addition to this, several single nucleotide polymorphisms in the HTR2A gene also predict clinical outcome, although molecular mechanisms remain unclear. Hence, the results indicate that while there is significant potential for predicting treatment response associated with these and other genetic targets, there is much work left to be done to establish conclusive evidence for and feasibility of pharmacogenetic testing.


Author(s):  
Oliver J. Robinson

Negative affective bias is a core symptom of major depressive disorder (MDD) that promotes and upholds the debilitating negative mood state. This chapter reviews cognitive neuroscience research exploring negative affective bias and its underlying neural circuitry. It describes converging research across clinical populations and experimental manipulations in humans suggesting that cortical and subcortical brain regions, and their interactions as circuits, are responsible for tipping the scales of information processing away from rewards and towards threats. The ultimate balance of activity within these neural circuits may therefore be responsible for negative affective bias symptoms in MDD.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yuhang Huan ◽  
Jing Wei ◽  
Jingjing Zhou ◽  
Min Liu ◽  
Jian Yang ◽  
...  

Major depressive disorder (MDD) is a common mental disorder that can cause substantial impairments in quality of life. Clinical treatment is usually built on a trial-and-error method, which lasts ~12 weeks to evaluate whether the treatment is efficient, thereby leading to some inefficient treatment measures. Therefore, we intended to identify early candidate urine biomarkers to predict efficient treatment response in MDD patients. In this study, urine samples were collected twice from 19 respondent and 10 non-respondent MDD patients receiving 0-, 2-, and 12-week treatments with escitalopram. Differential urinary proteins were subsequently analyzed by liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Our two pilot tests suggested that the urine proteome reflects changes associated with major depressive disorder at the early stage of treatment measures. On week 2, 20 differential proteins were identified in the response group compared with week 0, with 14 of these proteins being associated with the mechanisms of MDD. In the non-response group, 60 differential proteins were identified at week 2, with 28 of these proteins being associated with the mechanisms of MDD. In addition, differential urinary proteins at week 2 between the response and non-response groups can be clearly distinguished by using orthogonal projection on latent structure-discriminant analysis (OPLS-DA). Our small pilot tests indicated that the urine proteome can reflect early effects of escitalopram therapy between the response and non-response groups since at week 2, which may provide potential early candidate urine biomarkers to predict efficient treatment measures in MDD patients.


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