Re-evaluating the link between neuropsychiatric disorders and dysregulated adult neurogenesis

• Published in: Nature medicine Vol. 22; no. 11; pp. 1239 - 1247
• Main Authors: Yun, Sanghee, Reynolds, Ryan P, Masiulis, Irene, Eisch, Amelia J
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.11.2016; Nature Publishing Group
• Subjects: 631/136/2060/368/2431; 692/699/476; 692/699/476/1414; 692/699/476/1799; Abnormalities; Adult; Affect; Animal models; Animals; Anxiety Disorders - physiopathology; Biomedicine; Brain - physiopathology; Cancer Research; Dentate gyrus; Dentate Gyrus - cytology; Dentate Gyrus - physiopathology; Depressive Disorder - physiopathology; Development and progression; Humans; Infectious Diseases; Memory; Mental depression; Mental disorders; Mental Disorders - physiopathology; Metabolic Diseases; Molecular Medicine; Neurogenesis; Neurogenesis - physiology; Neurons; Neuropsychology; Neurosciences; perspective; Psychiatry; Reward; Risk factors; Schizophrenia - physiopathology; Substance-Related Disorders - physiopathology
• ISSN: 1078-8956; 1546-170X
• DOI: 10.1038/nm.4218

Recent evidence indicates that one of the underlying mechanisms in the pathogenesis of neuropsychiatric disorders is dysregulated dentate gyrus neurogenesis. Here the authors present evidence supporting this hypothesis and suggest therapeutic avenues. People diagnosed with neuropsychiatric disorders such as depression, anxiety, addiction or schizophrenia often have dysregulated memory, mood, pattern separation and/or reward processing. These symptoms are indicative of a disrupted function of the dentate gyrus (DG) subregion of the brain, and they improve with treatment and remission. The dysfunction of the DG is accompanied by structural maladaptations, including dysregulation of adult-generated neurons. An increasing number of studies using modern inducible approaches to manipulate new neurons show that the behavioral symptoms in animal models of neuropsychiatric disorders can be produced or exacerbated by the inhibition of DG neurogenesis. Thus, here we posit that the connection between neuropsychiatric disorders and dysregulated DG neurogenesis is beyond correlation or epiphenomenon, and that the regulation of adult-generated DG neurogenesis merits continued and focused attention in the ongoing effort to develop novel treatments for neuropsychiatric disorders.