Signalling mechanisms regulating neurogenesis and neurite outgrowth

创伤、中风、帕金森氏症、亨廷顿氏症和阿尔茨海默氏症等中枢神经系统(CNS)损伤和疾病每年影响相当数量的澳大利亚人，并往往对患者及其家人造成长期后果。这主要是由于对损害缺乏强有力的修复，以及缺乏可供治疗的治疗策略。然而，尽管还面临着许多障碍，但近年来出现了大量证据，这导致了一种观点，即在疾病损伤后修复中枢神经系统确实是可能的。有效的神经修复可能需要多因素的方法，包括阻断神经元死亡，用神经干细胞取代丢失的神经元，以及调节随后适当的轴突生长和正确连接的形成。我们已经证明，细胞因子信号调节因子SOCS2促进神经元分化和轴突生长。该项目旨在继续我们对SOCS2及其相互作用因素在调节神经元分化中的作用的研究，并利用体外和体内模型大幅扩展我们对SOCS2在调节轴突生长中的作用的研究。对这些过程中涉及的机制的了解可能会让我们获得损伤或疾病后神经系统修复的治疗方法。

Injury and diseases of the central nervous system (CNS), such as traumatic injury, stroke, Parkinson's, Huntington's and Alzheimer's disease, affect a substantial number of Australians each year and often have long-term consequences for sufferers and their families. This is primarily due to a lack of robust repair of the damage and a paucity of therapeutic strategies available for treatment. However, although many hurdles are yet to be faced, there is a substantial body of evidence that has emerged in recent years, that has led to the view that repair of the central nervous system following injury of disease may indeed be a possibility. Effective neural repair is likely to require a multi-factorial approach, including blockage of neuronal death, replacement of lost neurons by neural stem cells, and regulation of appropriate subsequent neurite outgrowth and formation of correct connections. We have shown that a regulator of cytokine signaling, SOCS2, promotes neuronal differentiation and neurite outgrowth. This project aims to continue our investigations of the role of SOCS2 and interacting factors in regulating neuronal differentiation as well as substantially expanding our investigations into the role of SOCS2 in regulating neurite outgrowth, using both in vitro and in vivo models. An understanding of the mechanisms involved in these processes may allow us to derive therapies for the repair of the nervous system after injury or disease.