Abstract
Major depressive disorder is characterized, among other symptoms, by depressed mood and anhedonia associated with a high rate of suicidal ideation. In recent years, research has shown reduced expression of the brain-derived neurotrophic factor (BDNF) in limbic areas of individuals with depression. This reduction of BDNF is reversed by antidepressants in animal models of stress. Stress is one of the main triggers of mood disorders such as depression. Also, administration of BDNF increases the number of serotonergic fibers and serotonergic innervation, indicating an increase of serotonin in the synaptic cleft by this neurotrophin. Thus, BDNF appears to be one of the targets of antidepressant drugs for the increase of monoamines and remission of symptoms of major depression. The purpose of this review was to show the evidence that indicates BDNF as a molecular substrate for vulnerability to depression and the response of this substrate to the antidepressants.
Highlights
Major depressive disorder is one of the most significant psychiatric disorders for public health worldwide
Treatment of major depression, which is associated with a high rate of suicidal ideation, resulting in about 15% death [3], includes electroconvulsive therapy, administration of psychoactive drugs such as lithium [34,35], tricyclic antidepressants, monoamine oxidase inhibitors (MAO), selective serotonin reuptake inhibitors (SSRIs) [36,37] and the use of certain substances such as L-tryptophan and L-5-hydroxytryptophan, which are present in some foods
Due to the clinical efficacy of antidepressant drugs arising after weeks of treatment or majority of patients failing to achieve complete remission, and as one third of them fail to respond to current drugs, new therapeutic targets are required for the clinical treatment of major depression disease [5]
Summary
Major depressive disorder is one of the most significant psychiatric disorders for public health worldwide. BDNF is one of the members of the neurotrophin family that among other functions promotes the maintenance and survival of neuronal cells [7,8]. This neurotrophin is reduced in depressed patients and in the post-mortem brain of victims of depression [9]. The data indicate that BDNF is intensely reduced in stress conditions, which is one of the main triggers of depression [9,10,11] and, in limbic areas such as hippocampus. The purpose of this review was to show the evidence that indicates BDNF as a molecular substrate for vulnerability to depression and the response of this substrate to antidepressants
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