论文部分内容阅读
近日,一项刊登在国际杂志Nature上的研究论文中,来自索尔克研究所和斯克利普斯研究所的研究人员通过研究揭示了突变的分子损伤腓骨肌萎缩症患者(CMT)神经系统的分子机制,CMT是一种影响个体移动能力及四肢感觉的机体障碍。实验室检测中,研究人员希望通过对小鼠进行研究可以改善腓骨肌萎缩症的症状,从而帮助开发新型CMT疾病的疗法。研究者指出,本文研究或为开发治疗CMT的新型药物提供潜在靶点,而且或许也为开发治疗其它神经变性疾病的新疗法提供思路。
Recently, in a research paper published in the journal Nature, Nature, researchers from the Salk Institute and the Scripps Research Institute revealed that mutated molecular damage in the nervous system of patients with Charcot-Marie-Tooth Syndrome (CMT) Molecular mechanisms, CMT is a body disorder that affects one’s mobility and limbs. In laboratory tests, the researchers hope that research on mice will improve the symptoms of Charcot-Marie Tooth Syndrome to help develop new CMT therapies. The researchers point out that this study may provide a potential target for the development of new drugs for the treatment of CMT and may also provide insights into the development of new therapies to treat other neurodegenerative diseases.