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

机译:BDNF / TrkB信号缺陷在神经系统和精神疾病中的整体表征为新疗法提供了途径

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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.
机译:脑源性神经营养因子(BDNF)信号的增强在治疗神经系统疾病和精神疾病方面具有巨大潜力。这种神经营养蛋白不仅可以减轻细胞死亡,还可以促进神经元的可塑性和功能。但是,这种方法的一个重要挑战是由于BDNF高亲和力受体,原肌球蛋白相关激酶B(TrkB)或下游效应子的功能缺陷,导致神经营养信号异常持续存在。已经在几种疾病中描述了这种变化,但是人们常常低估了它们作为病理机制的重要性。这篇综述强调了异常BDNF / TrkB途径的综合表征与合理设计疗法的相关性,通过结合BDNF和TrkB靶标可以有效促进神经营养信号传导。

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