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Neurotrophin-mediated neuroprotection of hippocampal neurons following traumatic brain injury is not associated with acute recovery of hippocampal function.神经营养因子介导的创伤性脑损伤后海马神经元神经保护作用与海马功能的急性恢复无关。
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Advances in small molecules promoting neurotrophic function.促进神经营养功能的小分子研究进展。
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The failure in NGF maturation and its increased degradation as the probable cause for the vulnerability of cholinergic neurons in Alzheimer's disease.神经生长因子（NGF）成熟过程中的失败及其降解增加可能是阿尔茨海默病中胆碱能神经元易损性的原因。
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Injury-induced axonal sprouting in the hippocampus is initiated by activation of trkB receptors.海马体中由损伤诱导的轴突萌发是由trkB受体的激活引发的。
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On the molecular basis linking Nerve Growth Factor (NGF) to Alzheimer's disease.将神经生长因子（NGF）与阿尔茨海默病联系起来的分子基础。
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用于神经保护的Trk受体小分子激活剂。

Small molecule activators of the Trk receptors for neuroprotection.

作者信息

Webster Nicholas J G, Pirrung Michael C

机构信息

Veterans Medical Research Foundation and VA San Diego Healthcare System, San Diego, CA 92161, USA.

出版信息

BMC Neurosci. 2008 Dec 3;9 Suppl 2(Suppl 2):S1. doi: 10.1186/1471-2202-9-S2-S1.

DOI:10.1186/1471-2202-9-S2-S1
PMID:19090982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2604901/
Abstract

The neurotrophin signaling network is critical to the development and survival of many neuronal populations. Especially sensitive to imbalances in the neurotrophin system, cholinergic neurons in the basal forebrain are progressively lost in Alzheimer's disease. Therapeutic use of neurotrophins to prevent this loss is hampered, however, by a number of pharmacological challenges. These include a lack of transport across the blood-brain barrier, rapid degradation in the circulation, and difficulty in production. In this review we discuss the evidence supporting the neurotrophin system's role in preventing neurodegeneration and survey some of the pharmacological strategies being pursued to develop effective therapeutics targeting neurotrophin function.

摘要

神经营养因子信号网络对于许多神经元群体的发育和存活至关重要。基底前脑的胆碱能神经元对神经营养因子系统的失衡尤为敏感，在阿尔茨海默病中会逐渐丧失。然而，神经营养因子在治疗上用于预防这种丧失却受到一些药理学挑战的阻碍。这些挑战包括无法穿过血脑屏障、在循环中快速降解以及生产困难。在本综述中，我们讨论了支持神经营养因子系统在预防神经退行性变中作用的证据，并概述了为开发针对神经营养因子功能的有效疗法而正在探索的一些药理学策略。