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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Facchinetti F, Dawson V L, Dawson T M

Department of Neurology, Neuroscience and Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.

Cell Mol Neurobiol. 1998 Dec;18(6):667-82. doi: 10.1023/a:1020685903186.

Free radicals may play an important role in several pathological conditions of the central nervous system (CNS) where they directly injure tissue and where their formation may also be a consequence of tissue injury. 2. Free radicals produce tissue damage through multiple mechanisms, including excito-toxicity, metabolic dysfunction, and disturbance of intracellular homeostasis of calcium. 3. Oxidative stress can significantly worsen acute insults, such as ischemia, as well as chronic neurodegenerative disorders including amyotrophic lateral sclerosis (ALS) and Parkinson's disease. 4. For instance, recent findings suggest a causal role for chronic oxidative stress in familial ALS, as this disease is linked to missence mutations of the copper/zinc superoxide dismutase (SOD). 5. Thus, therapeutic approaches which limit oxidative stress may be potentially beneficial in several neurological diseases.

自由基可能在中枢神经系统（CNS）的多种病理状况中发挥重要作用，在这些状况下它们直接损伤组织，并且其形成也可能是组织损伤的结果。2. 自由基通过多种机制造成组织损伤，包括兴奋毒性、代谢功能障碍以及细胞内钙稳态的紊乱。3. 氧化应激可显著加重急性损伤，如局部缺血，以及慢性神经退行性疾病，包括肌萎缩侧索硬化症（ALS）和帕金森病。4. 例如，最近的研究结果表明慢性氧化应激在家族性ALS中起因果作用，因为这种疾病与铜/锌超氧化物歧化酶（SOD）的错义突变有关。5. 因此，限制氧化应激的治疗方法可能对几种神经系统疾病具有潜在益处。

Facchinetti F, Dawson V L, Dawson T M

Department of Neurology, Neuroscience and Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.

Cell Mol Neurobiol. 1998 Dec;18(6):667-82. doi: 10.1023/a:1020685903186.

Free radicals may play an important role in several pathological conditions of the central nervous system (CNS) where they directly injure tissue and where their formation may also be a consequence of tissue injury. 2. Free radicals produce tissue damage through multiple mechanisms, including excito-toxicity, metabolic dysfunction, and disturbance of intracellular homeostasis of calcium. 3. Oxidative stress can significantly worsen acute insults, such as ischemia, as well as chronic neurodegenerative disorders including amyotrophic lateral sclerosis (ALS) and Parkinson's disease. 4. For instance, recent findings suggest a causal role for chronic oxidative stress in familial ALS, as this disease is linked to missence mutations of the copper/zinc superoxide dismutase (SOD). 5. Thus, therapeutic approaches which limit oxidative stress may be potentially beneficial in several neurological diseases.

自由基可能在中枢神经系统（CNS）的多种病理状况中发挥重要作用，在这些状况下它们直接损伤组织，并且其形成也可能是组织损伤的结果。2. 自由基通过多种机制造成组织损伤，包括兴奋毒性、代谢功能障碍以及细胞内钙稳态的紊乱。3. 氧化应激可显著加重急性损伤，如局部缺血，以及慢性神经退行性疾病，包括肌萎缩侧索硬化症（ALS）和帕金森病。4. 例如，最近的研究结果表明慢性氧化应激在家族性ALS中起因果作用，因为这种疾病与铜/锌超氧化物歧化酶（SOD）的错义突变有关。5. 因此，限制氧化应激的治疗方法可能对几种神经系统疾病具有潜在益处。