Citation

Gulbins E, Walter S, Becker KA, Halmer R, Liu Y, Reichel M, Edwards MJ, Müller CP, Fassbender K, Kornhuber J. J. Neurochem. 2015; 134(2): 183-192.

Affiliation

Department of Molecular Biology, University of Duisburg-Essen, Hufelandstrasse 55, 45122, Essen, Germany; Department of Surgery, University of Cincinnati, Cincinnati, OH, 45267, USA.

Copyright

(Copyright © 2015, John Wiley and Sons)

DOI

10.1111/jnc.13145

PMID

25925550

Abstract

Major depressive disorder is a severe and chronic illness with high lifetime prevalence and a high incidence of suicide as the cause of death for patients with this diagnosis. Major depressive disorder is often treated with antidepressants. Although these drugs have been used for many years, their exact mode of action is still unknown. It has been suggested that many antidepressants act by increasing the concentrations of serotonergic transmitters in the synaptic space. However, recent studies have examined the effects of antidepressants on neurogenesis in the hippocampus, the restoration of hippocampal neuronal networks that may be affected by major depression, and the regulation of the hypothalamic-pituitary-adrenal axis by immature neurons in the hippocampus. Here we present and discuss a novel hypothesis suggesting that these events are regulated by the concentrations of sphingolipids, in particular ceramide, in the hippocampus. These concepts suggest that the acid sphingomyelinase/ceramide system plays a central role in the pathogenesis of major depression and may be a novel target for antidepressants. This article is protected by copyright. All rights reserved.

Language: en