Wong Philip C, Cai Huaibin, Borchelt David R, Price Donald L
Department of Pathology, The Johns Hopkins University School of Medicine, 558 Ross Research Building, 720 Rutland Avenue, Baltimore, Maryland 21205-2196, USA.
Nat Neurosci. 2002 Jul;5(7):633-9. doi: 10.1038/nn0702-633.
Recent research has significantly advanced our understanding of the molecular mechanisms of neurodegenerative diseases, including Alzheimer's disease (AD) and motor neuron disease. Here we emphasize the use of genetically engineered mouse models that are instrumental for understanding why AD is a neuronal disease, and for validating attractive therapeutic targets. In motor neuron diseases, Cu/Zn superoxide dismutase and survival motor neuron mouse models are useful in testing disease mechanisms and therapeutic strategies for amyotrophic lateral sclerosis (ALS) and spinal motor atrophy, respectively, but the mechanisms that account for selective motor neuron loss remain uncertain. We anticipate that, in the future, therapies based on understanding disease mechanisms will be identified and tested in mouse model systems.
最近的研究极大地推进了我们对神经退行性疾病分子机制的理解,这些疾病包括阿尔茨海默病(AD)和运动神经元病。在此,我们强调使用基因工程小鼠模型,这些模型有助于理解AD为何是一种神经元疾病,并有助于验证有吸引力的治疗靶点。在运动神经元疾病中,铜/锌超氧化物歧化酶和存活运动神经元小鼠模型分别有助于测试肌萎缩侧索硬化症(ALS)和脊髓性肌萎缩症的疾病机制及治疗策略,但导致选择性运动神经元丢失的机制仍不明确。我们预计,未来将基于对疾病机制的理解来确定治疗方法,并在小鼠模型系统中进行测试。