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在1993年通过对细胞质内铜/锌(Cu/Zn)超氧化物歧化酶(SOD_1)突变的观察与肌萎缩侧索硬化症(ALS)的一些家族类型(FALS)有关,提出本病是由体内自由基平衡紊乱及通过活性氧形式产生神经细胞毒性。作者就此提出了一些新观点,提出本病并不是由于SOD_1的损耗引起,相反是由变异SOD_1分子具有相悖或异常的特性引起。新进两个研究在叙述有毒化学反应首先与变异SOD_1酶相关方面取得了令人兴奋的进展。其一是Beckman提出变异SOD_1分子实际上是化合物基
In 1993, the observation that the cytoplasmic Cu / Zn superoxide dismutase (SOD1) mutation was associated with some familial types of amyotrophic lateral sclerosis (ALS) suggests that the disease is caused by Free radical balance in the body and neurotoxicity via reactive oxygen species. The authors put forward some new ideas in this regard, suggesting that the disease is not caused by the depletion of SOD_1, but rather by the contradictory or abnormal characteristics of mutant SOD_1 molecules. Two new advances have made exciting progress in describing the first toxic chemical reaction associated with the mutant SOD-1 enzyme. One is that Beckman proposed that mutant SOD_1 molecules are actually compound based