Towne Chris, Aebischer Patrick
Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Methods Mol Biol. 2009;555:87-108. doi: 10.1007/978-1-60327-295-7_7.
RNAi holds promise for neurodegenerative disorders caused by gain-of-function mutations. We and others have demonstrated proof-of-principle for viral-mediated RNAi in a mouse model of motor neuron disease. Lentivirus and adeno-associated virus have been used to knockdown levels of mutated superoxide dismutase 1 (SOD1) in the G93A SOD1 mouse model of familial amyotrophic lateral sclerosis (fALS) to result in beneficial therapeutic outcomes. This chapter describes the design, production, and titration of lentivirus and adeno-associated virus capable of mediating SOD1 knockdown in vivo. The delivery of the virus to the spinal cord directly, through intraspinal injection, or indirectly, through intramuscular injection, is also described, as well as the methods pertaining to the analysis of spinal cord transduction, SOD1 silencing, and determination of motor neuron protection.
RNA干扰技术有望用于治疗由功能获得性突变引起的神经退行性疾病。我们和其他研究人员已经在运动神经元疾病的小鼠模型中证明了病毒介导的RNA干扰技术的原理。在家族性肌萎缩侧索硬化症(fALS)的G93A超氧化物歧化酶1(SOD1)小鼠模型中,慢病毒和腺相关病毒已被用于降低突变型SOD1的水平,从而产生有益的治疗效果。本章描述了能够在体内介导SOD1基因敲低的慢病毒和腺相关病毒的设计、生产和滴定。还介绍了通过脊髓内注射直接将病毒递送至脊髓,或通过肌肉注射间接递送病毒的方法,以及与脊髓转导分析、SOD1沉默和运动神经元保护测定相关的方法。