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Int. J. Mol. Sci. 2017, 18(2), 268; doi:10.3390/ijms18020268

Integral Characterization of Defective BDNF/TrkB Signalling in Neurological and Psychiatric Disorders Leads the Way to New Therapies

Instituto de Investigaciones Biomédicas “Alberto Sols”, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Arturo Duperier 4, 28029 Madrid, Spain
Present address: Gardiner Laboratory, Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, Scotland, UK
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Author to whom correspondence should be addressed.
Received: 30 December 2016 / Revised: 15 January 2017 / Accepted: 23 January 2017 / Published: 28 January 2017
(This article belongs to the Special Issue Brain-Derived Neurotrophic Factor)
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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. View Full-Text
Keywords: BDNF; TrkB; excitotoxicity; stroke; neurodegeneration; neuroprotection; therapy BDNF; TrkB; excitotoxicity; stroke; neurodegeneration; neuroprotection; therapy
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Tejeda, G.S.; Díaz-Guerra, M. Integral Characterization of Defective BDNF/TrkB Signalling in Neurological and Psychiatric Disorders Leads the Way to New Therapies. Int. J. Mol. Sci. 2017, 18, 268.

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