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脑源性神经营养因子-酪氨酸激酶受体B信号通路的调控及帕金森病的潜在治疗策略

Regulation of BDNF-TrkB Signaling and Potential Therapeutic Strategies for Parkinson's Disease.

作者信息

Jin Wook

机构信息

Laboratory of Molecular Disease and Cell Regulation, Department of Biochemistry, School of Medicine, Gachon University, Incheon 21999, Korea.

出版信息

J Clin Med. 2020 Jan 17;9(1):257. doi: 10.3390/jcm9010257.

DOI:10.3390/jcm9010257
PMID:31963575
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7019526/
Abstract

Brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase receptor type B (TrkB) are widely distributed in multiple regions of the human brain. Specifically, BDNF/TrkB is highly expressed and activated in the dopaminergic neurons of the substantia nigra and plays a critical role in neurophysiological processes, including neuro-protection and maturation and maintenance of neurons. The activation as well as dysfunction of the BDNF-TrkB pathway are associated with neurodegenerative diseases. The expression of BDNF/TrkB in the substantia nigra is significantly reduced in Parkinson's Disease (PD) patients. This review summarizes recent progress in the understanding of the cellular and molecular roles of BNDF/TrkB signaling and its isoform, TrkB.T1, in Parkinson's disease. We have also discussed the effects of current therapies on BDNF/TrkB signaling in Parkinson's disease patients and the mechanisms underlying the mutation-mediated acquisition of resistance to therapies for Parkinson's disease.

摘要

脑源性神经营养因子（BDNF）及其受体原肌球蛋白相关激酶B型受体（TrkB）广泛分布于人类大脑的多个区域。具体而言，BDNF/TrkB在黑质的多巴胺能神经元中高表达并被激活，在神经生理过程中发挥关键作用，包括神经保护以及神经元的成熟与维持。BDNF-TrkB通路的激活以及功能障碍与神经退行性疾病相关。在帕金森病（PD）患者中，黑质中BDNF/TrkB的表达显著降低。本综述总结了在理解BDNF/TrkB信号及其异构体TrkB.T1在帕金森病中的细胞和分子作用方面的最新进展。我们还讨论了当前疗法对帕金森病患者BDNF/TrkB信号的影响以及帕金森病治疗耐药性突变介导获得的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54a/7019526/02f4333e21d0/jcm-09-00257-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54a/7019526/bac532f28634/jcm-09-00257-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54a/7019526/345c32910268/jcm-09-00257-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54a/7019526/cb46994d0268/jcm-09-00257-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54a/7019526/02f4333e21d0/jcm-09-00257-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54a/7019526/bac532f28634/jcm-09-00257-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54a/7019526/345c32910268/jcm-09-00257-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54a/7019526/cb46994d0268/jcm-09-00257-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54a/7019526/02f4333e21d0/jcm-09-00257-g004.jpg

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