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脑源性神经营养因子在成体突触可塑性中的机制与功能:新见解及治疗意义

Brain-derived neurotrophic factor mechanisms and function in adult synaptic plasticity: new insights and implications for therapy.

作者信息

Kuipers Sjoukje D, Bramham Clive R

机构信息

Department of Biomedicine and Bergen Mental Health Research Center, University of Bergen, Jonas Lies vei 91, N-5009 Bergen, Norway.

出版信息

Curr Opin Drug Discov Devel. 2006 Sep;9(5):580-6.

Abstract

Synaptic plasticity, the fiundamental ability of synapses to undergo experience-dependent changes in synaptic strength, is thought to underlie a range of long-term adaptive responses of the central nervous system. The inability to generate or maintain appropriate changes in synaptic connectivity and neuronal circuitry is likely to impair cognitive futnction associated with many neurological and psychiatric disorders. The success of intervening therapeutic approaches will depend on the ability to target key component mechanisms in the complex process of synaptic plasticity. Brain-derived neurotrophic factor (BDNF) has emerged as a major regulator of synaptic plasticity and a key target in disorders such as major depression and Alzheimner's disease. This review discusses findings that link BDNF mechanisms in synaptic plasticity to disease mechanisms and possible future therapies.

摘要

突触可塑性是突触经历依赖于经验的突触强度变化的基本能力,被认为是中枢神经系统一系列长期适应性反应的基础。无法在突触连接和神经元回路中产生或维持适当的变化可能会损害与许多神经和精神疾病相关的认知功能。干预性治疗方法的成功将取决于在复杂的突触可塑性过程中靶向关键组成机制的能力。脑源性神经营养因子(BDNF)已成为突触可塑性的主要调节因子,也是重度抑郁症和阿尔茨海默病等疾病的关键靶点。本综述讨论了将BDNF在突触可塑性中的机制与疾病机制及未来可能的治疗方法联系起来的研究结果。

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