@article{ref1,
title="Direct and indirect evidences of BDNF and NGF as key modulators in depression: role of antidepressants treatment",
journal="International journal of neuroscience",
year="2019",
author="Mondal, Amal Chandra and Fatima, Mahino",
volume="129",
number="3",
pages="283-296",
abstract="Depression is one of the most prevalent, recurrent and life-threatening mental illnesses. However, the precise mechanism underlying the disorder is not understood yet. It is therefore, essential to identify the symptoms and then discover the novel biomarkers which will help in the diagnosis and the development of effective treatment. In this milieu, number of preclinical and clinical studies suggest that several neurotrophic factors, including the brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) play an important role in the pathophysiology of major depression. Previously, we have reported that BDNF level in the brain of suicide victims was significantly lower than those of normal controls. We have also shown decreased BDNF levels in the specific brain regions of the learned helplessness model of depression in rat. This was increased to the normal level following chronic fluoxetine hydrochloride treatment. NGF is another important neurotrophin, which is dysregulated in the pathophysiology of depression in some animal models of peripheral nerve damage and stress. But some recent results have shown conflicted preclinical and clinical evidences on the effect of ADs treatment on modulating depression via NGF, therefore making it difficult to affirm the therapeutic role of antidepressants (ADs). Here, we review some of the preclinical and clinical studies aimed at disclosing the role of BDNF and NGF mediating pathophysiological mechanisms of depression and the new therapeutic approaches targeting these molecules. In addition, an important link between BDNF, NGF in depression and ADs treatment has been discussed in the light of current existing knowledge.<p /> <p>Language: en</p>",
language="en",
issn="0020-7454",
doi="10.1080/00207454.2018.1527328",
url="http://dx.doi.org/10.1080/00207454.2018.1527328"
}