The role of axon guidance molecules in the pathogenesis of epilepsy.

IF 5.9 2区 医学 Q2 CELL BIOLOGY Neural Regeneration Research Pub Date : 2025-05-01 Epub Date: 2024-04-16 DOI:10.4103/NRR.NRR-D-23-01620
Zheng Liu, Chunhua Pan, Hao Huang
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Abstract

Current treatments for epilepsy can only manage the symptoms of the condition but cannot alter the initial onset or halt the progression of the disease. Consequently, it is crucial to identify drugs that can target novel cellular and molecular mechanisms and mechanisms of action. Increasing evidence suggests that axon guidance molecules play a role in the structural and functional modifications of neural networks and that the dysregulation of these molecules is associated with epilepsy susceptibility. In this review, we discuss the essential role of axon guidance molecules in neuronal activity in patients with epilepsy as well as the impact of these molecules on synaptic plasticity and brain tissue remodeling. Furthermore, we examine the relationship between axon guidance molecules and neuroinflammation, as well as the structural changes in specific brain regions that contribute to the development of epilepsy. Ample evidence indicates that axon guidance molecules, including semaphorins and ephrins, play a fundamental role in guiding axon growth and the establishment of synaptic connections. Deviations in their expression or function can disrupt neuronal connections, ultimately leading to epileptic seizures. The remodeling of neural networks is a significant characteristic of epilepsy, with axon guidance molecules playing a role in the dynamic reorganization of neural circuits. This, in turn, affects synapse formation and elimination. Dysregulation of these molecules can upset the delicate balance between excitation and inhibition within a neural network, thereby increasing the risk of overexcitation and the development of epilepsy. Inflammatory signals can regulate the expression and function of axon guidance molecules, thus influencing axonal growth, axon orientation, and synaptic plasticity. The dysregulation of neuroinflammation can intensify neuronal dysfunction and contribute to the occurrence of epilepsy. This review delves into the mechanisms associated with the pathogenicity of axon guidance molecules in epilepsy, offering a valuable reference for the exploration of therapeutic targets and presenting a fresh perspective on treatment strategies for this condition.

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轴突导向分子在癫痫发病机制中的作用。
目前治疗癫痫的方法只能控制病情的症状,但无法改变最初的发病或阻止病情的发展。因此,找出能够针对新型细胞和分子机制及作用机制的药物至关重要。越来越多的证据表明,轴突导向分子在神经网络的结构和功能改变中发挥作用,而这些分子的失调与癫痫易感性有关。在这篇综述中,我们将讨论轴突导向分子在癫痫患者神经元活动中的重要作用,以及这些分子对突触可塑性和脑组织重塑的影响。此外,我们还研究了轴突导向分子与神经炎症之间的关系,以及导致癫痫发生的特定脑区结构变化。大量证据表明,轴突导向分子(包括semaphorins和ephrins)在引导轴突生长和建立突触连接方面发挥着重要作用。它们的表达或功能偏差会破坏神经元连接,最终导致癫痫发作。神经网络的重塑是癫痫的一个重要特征,轴突导向分子在神经回路的动态重组中发挥着作用。这反过来又会影响突触的形成和消除。这些分子的失调会破坏神经网络内兴奋和抑制之间的微妙平衡,从而增加过度兴奋和发展成癫痫的风险。炎症信号可调节轴突导向分子的表达和功能,从而影响轴突生长、轴突定向和突触可塑性。神经炎症的失调会加剧神经元功能障碍,导致癫痫的发生。这篇综述深入探讨了轴突导向分子在癫痫中的致病机制,为探索治疗靶点提供了宝贵的参考,并为该疾病的治疗策略提供了全新的视角。
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来源期刊
Neural Regeneration Research
Neural Regeneration Research CELL BIOLOGY-NEUROSCIENCES
CiteScore
8.00
自引率
9.80%
发文量
515
审稿时长
1.0 months
期刊介绍: Neural Regeneration Research (NRR) is the Open Access journal specializing in neural regeneration and indexed by SCI-E and PubMed. The journal is committed to publishing articles on basic pathobiology of injury, repair and protection to the nervous system, while considering preclinical and clinical trials targeted at improving traumatically injuried patients and patients with neurodegenerative diseases.
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