Department of Cell Biology, Neurobiology, and Anatomy, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Department of Neurology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Cells. 2020 Feb 28;9(3):571. doi: 10.3390/cells9030571.
Amyotrophic lateral sclerosis (ALS) is a complex neurodegenerative disorder characterized by the loss of the upper and lower motor neurons. Approximately 10% of cases are caused by specific mutations in known genes, with the remaining cases having no known genetic link. As such, sporadic cases have been more difficult to model experimentally. Here, we describe the generation and differentiation of ALS induced pluripotent stem cells reprogrammed from discordant identical twins. Whole genome sequencing revealed no relevant mutations in known ALS-causing genes that differ between the twins. As protein aggregation is found in all ALS patients and is thought to contribute to motor neuron death, we sought to characterize the aggregation phenotype of the sporadic ALS induced pluripotent stem cells (iPSCs). Motor neurons from both twins had high levels of insoluble proteins that commonly aggregate in ALS that did not robustly change in response to exogenous glutamate. In contrast, established genetic ALS iPSC lines demonstrated insolubility in a protein- and genotype-dependent manner. Moreover, whereas the genetic ALS lines failed to induce autophagy after glutamate stress, motor neurons from both twins and independent controls did activate this protective pathway. Together, these data indicate that our unique model of sporadic ALS may provide key insights into disease pathology and highlight potential differences between sporadic and familial ALS.
肌萎缩侧索硬化症(ALS)是一种复杂的神经退行性疾病,其特征是上运动神经元和下运动神经元的丧失。大约 10%的病例是由已知基因的特定突变引起的,其余病例则没有已知的遗传联系。因此,散发性病例在实验上更难建模。在这里,我们描述了从不一致的同卵双胞胎中重新编程的肌萎缩侧索硬化症诱导多能干细胞的生成和分化。全基因组测序显示,双胞胎之间不同的、已知会引起 ALS 的基因中没有相关突变。由于蛋白聚集存在于所有 ALS 患者中,并被认为导致运动神经元死亡,因此我们试图描述散发性肌萎缩侧索硬化症诱导多能干细胞(iPSC)的聚集表型。来自双胞胎的运动神经元都有高水平的不溶性蛋白,这些蛋白通常在 ALS 患者中聚集,并且对外源谷氨酸没有强烈的反应。相比之下,已建立的遗传 ALS iPSC 系以蛋白和基因型依赖的方式表现出不溶性。此外,虽然遗传 ALS 系在谷氨酸应激后不能诱导自噬,但来自双胞胎和独立对照的运动神经元都激活了这种保护途径。总之,这些数据表明,我们独特的散发性 ALS 模型可能为疾病病理学提供重要的见解,并突出散发性和家族性 ALS 之间的潜在差异。