Integral characterization of defective BDNF/TrkB signalling in neurological and psychiatric disorders leads the way to new therapies

Tejeda, G. and Díaz-Guerra, M. (2017) Integral characterization of defective BDNF/TrkB signalling in neurological and psychiatric disorders leads the way to new therapies. International Journal of Molecular Sciences, 18(2), 268. (doi: 10.3390/ijms18020268) (PMID:28134845) (PMCID:PMC5343804)

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Abstract

Enhancement of brain-derived neurotrophic factor (BDNF) signalling has great potential in therapy for neurological and psychiatric disorders. This neurotrophin not only attenuates cell death but also promotes neuronal plasticity and function. However, an important challenge to this approach is the persistence of aberrant neurotrophic signalling due to a defective function of the BDNF high-affinity receptor, tropomyosin-related kinase B (TrkB), or downstream effectors. Such changes have been already described in several disorders, but their importance as pathological mechanisms has been frequently underestimated. This review highlights the relevance of an integrative characterization of aberrant BDNF/TrkB pathways for the rational design of therapies that by combining BDNF and TrkB targets could efficiently promote neurotrophic signalling.

Item Type:Articles
Additional Information:We acknowledge funding from Ministerio de Economía y Competitividad (BFU2013-43808-R) and Fundación Mutua Madrileña (reference No. 201322001). The cost of this publication has been paid in part by FEDER funds.
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Tejeda, Dr Gonzalo
Authors: Tejeda, G., and Díaz-Guerra, M.
College/School:College of Medical Veterinary and Life Sciences > School of Cardiovascular & Metabolic Health
Journal Name:International Journal of Molecular Sciences
Publisher:MDPI
ISSN:1661-6596
ISSN (Online):1422-0067
Published Online:28 January 2017
Copyright Holders:Copyright © 2018 The Authors
First Published:First published in International Journal of Molecular Sciences 18(2):268
Publisher Policy:Reproduced under a Creative Commons License

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