About this Research Topic
Depression is a serious mental illness with high prevalence, high relapse rates, high disease burden, and high suicide mortality. The World Health Organization predicts that by 2030, depression will become the first global disease burden. To date, the etiology of depression is unknown and the pathogenesis is complex. Various hypotheses have been proposed for the pathogenesis of depression, including the well-known neuroinflammatory hypothesis and the classical neurotransmitter system dysregulation hypothesis. Clinical antidepressant drugs are mainly developed for neurotransmitter targets, and such drugs have problems such as slow onset of action, large side effects, easy relapse after discontinuation, and addiction and hallucinogenicity. Currently, most of the drugs developed against neuroinflammatory targets are ineffective and their clinical trials have failed. Therefore, there is an urgent need to find new mechanisms and targets of neuroinflammation to provide new ideas and directions for clinical antidepressant treatment.
Microglia and astrocytes, as important immune cells, are the main source of neuroinflammation, and their malfunction is involved in the pathogenesis of depression. A large number of articles related to the neuroinflammatory mechanisms of depression have been published. However, there is still no clinical drug that has been developed for neuroinflammation. Therefore, in order to advance the study of neuroinflammatory mechanisms of depression and the discovery of antidepressant drugs, we aim to pursue the topic of neuroinflammatory mechanisms associated with depression.
We highly encourage addressing specific themes that encompass, but are not limited to, the following:
1. morphological and functional studies of microglia and astrocytes in depression;
2. the effect of the interaction of microglia and astrocytes on depression;
3. the effect of the interaction of microglia and neurons on depression;
4. the effect of interactions between astrocytes and neurons on depression;
5. mechanistic studies of neuroinflammation and depression;
6. drug studies on neuroinflammatory targets for depression;
7. studies on neuroinflammatory aspects in clinical samples of depressed patients.
Microglia and astrocytes, as important immune cells, are the main source of neuroinflammation, and their malfunction is involved in the pathogenesis of depression. A large number of articles related to the neuroinflammatory mechanisms of depression have been published. However, there is still no clinical drug that has been developed for neuroinflammation. Therefore, in order to advance the study of neuroinflammatory mechanisms of depression and the discovery of antidepressant drugs, we aim to pursue the topic of neuroinflammatory mechanisms associated with depression.
We highly encourage addressing specific themes that encompass, but are not limited to, the following:
1. morphological and functional studies of microglia and astrocytes in depression;
2. the effect of the interaction of microglia and astrocytes on depression;
3. the effect of the interaction of microglia and neurons on depression;
4. the effect of interactions between astrocytes and neurons on depression;
5. mechanistic studies of neuroinflammation and depression;
6. drug studies on neuroinflammatory targets for depression;
7. studies on neuroinflammatory aspects in clinical samples of depressed patients.
Keywords: Depression, Neuroinflammation, Microglia, Astrocytes, Clinical antidepressant drugs
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
