Targeting autophagy to counteract neuroinflammation: A novel antidepressant strategy

Abstract

Depression is a common disease that affects physical and mental health and imposes a considerable burden on afflicted individuals and their families worldwide. Depression is associated with a high rate of disability and suicide. It causes a severe decline in productivity and quality of life. Unfortunately, the pathophysiological mechanisms underlying depression have not been fully elucidated, and the risk of its treatment is still presented. Studies have shown that the expression of autophagic markers in the brain and peripheral inflammatory mediators are dysregulated in depression. Autophagy-related genes regulate the level of autophagy and change the inflammatory response in depression. Depression is related to several aspects of immunity. The regulation of the immune system and inflammation by autophagy may lead to the development or deterioration of mental disorders. This review highlights the role of autophagy and neuroinflammation in the pathophysiology of depression, sumaries the autophagy-targeting small moleculars, and discusses a novel therapeutic strategy based on anti-inflammatory mechanisms that target autophagy to treat the disease.

Keywords: (-)-Epigallocatechin-3-O-gallate (Pubchem CID: 65064); Agomelatine (Pubchem CID: 82148); Andrographolide (Pubchem CID: 5318517); Aucubin (Pubchem CID: 91458); Autophagy; Bafilomycin A1 (Pubchem CID: 6436223); Canagliflozin (Pubchem CID: 24812758); Depression; Eicosapentaenoic acid (Pubchem CID: 446284); Exendin-4 (Pubchem CID: 45588096); Ginsenoside Rb1 (Pubchem CID: 9898279); Hyperforin (Pubchem CID: 441298); Neuroinflammation; Pathophysiology; Small molecular.