Overexpression of neuronal calcium sensor-1 to promote axonal regeneration

神经元钙传感器1的过度表达促进轴突再生

• 批准号: G0501617/1
• 负责人: Stephen McMahon
• 金额: $ 41.79万
• 依托单位: King's College London
• 依托单位国家: 英国
• 项目类别: Research Grant
• 财政年份: 2006
• 资助国家: 英国
• 起止时间: 2006 至 无数据
• 项目状态: 已结题
• 来源: https://gtr.ukri.org/projects?ref=G0501617%2F1
• 关键词: Overexpression; neuronal; calcium; sensor; promote

Patients with spinal cord injury (SCI) are often left with severe sensory, motor and autonomic functional deficits. In the proposed research we aim to test the hypothesis that adding a calcium sensor protein; neuronal calcium sensor-1 (NCS-1) can enable adult nerves to regenerate. This small molecule is involved in the growth of axons and formation of synapses (the wiring and communication points of nerves) in the embryonic brain and spinal cord. This molecule is usually only expressed in the embryonic nervous system which, as well as normal growth, is also capable of significant regeneration after injury. We plan to increase the NCS-1 content of injured nerves in two models of SCI in the adult rat. The differences between the two models will allow us to examine the contribution of different mechanisms that may underlie any functional recovery caused by the increase in NCS-1. Clinically the treatment of the neuronal injury following SCI is delayed by the need to stabilise the patient, therefore we will test if increasing NCS-1 after as opposed to at the same time as the injury can induce recovery. We hope this work may contribute to new treatment options in SCI.

脊髓损伤（SCI）患者通常会留下严重的感觉、运动和自主神经功能缺陷。在提出的研究中，我们旨在验证添加钙传感器蛋白的假设；神经元钙传感器-1 （neural calcium sensor-1, NCS-1）能够促进成体神经的再生。这种小分子参与了胚胎大脑和脊髓中轴突的生长和突触（神经的连接和交流点）的形成。这种分子通常只在胚胎神经系统中表达，胚胎神经系统和正常生长的神经系统一样，在损伤后也有显著的再生能力。我们计划在两种成年大鼠脊髓损伤模型中增加NCS-1的含量。两种模型之间的差异将使我们能够检查不同机制的贡献，这些机制可能是NCS-1增加引起的任何功能恢复的基础。临床上对脊髓损伤后神经元损伤的治疗因需要稳定患者而延迟，因此我们将测试在损伤后而不是同时增加NCS-1是否可以诱导恢复。我们希望这项工作能为脊髓损伤的治疗提供新的选择。