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mTOR Signaling and Depression Published by Dove Medical Press
Date:12/8/2015

The Journal of Receptor, Ligand and Channel Research has published the review “mTOR signaling in the neuropathophysiology of depression: current evidence”.

As corresponding author Dr Ana Lúcia Rodrigues says “The review by Reus et al deals with the role of mammalian target of rapamycin (mTOR) signaling in the neuropathophysiology of depression. A special focus is given to ketamine, a fast-acting antidepressant that elicits its antidepressant effect by activating this pathway in prefrontal cortex and hippocampus. This forms the basis for the review which evaluates mTOR as a neurobiological feature of depression and as a target for antidepressant treatment.”

Dr Rodrigues continues “It is concluded that a better understanding on the role of mTOR signaling in different brain regions and its upstream and downstream targets may provide novel insights into the development of therapeutic approaches for the management of depression.”

As Professor Trevor W. Stone, Editor-in-Chief, explains “The search for effective but safe anti-depressant drugs continues in parallel with studies of dietary influences and the use of lifestyle factors such as exercise. In this short review Rodrigues and colleagues summarise key findings on these topics and draw together the evidence that they may act via a common pathway known as mTOR (mammalian Target Of Rapamycin). A more intensive investigation into this target could yield the more selective and useful drugs that are urgently needed.”

The Journal of Receptor, Ligand and Channel Research is an international, peer-reviewed, open access, online journal. The journal welcomes laboratory and clinical findings in the fields of biological receptors, ligands, channel and signal transduction research.

Dove Medical Press Ltd is a privately held company specializing in the publication of Open Access peer-reviewed journals across the broad spectrum of science, technology and especially medicine.

Read the full story at http://www.prweb.com/releases/2015/12/prweb13118848.htm.


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