Myszczynska Monika, Ferraiuolo Laura
Department of Neuroscience, Sheffield Institute for Translational Neuroscience, University of Sheffield, UK.
Brain Pathol. 2016 Mar;26(2):258-65. doi: 10.1111/bpa.12353.
Amyotrophic Lateral Sclerosis (ALS) is a complex multifactorial disorder, characterized by motor neuron loss with involvement of several other cell types, including astrocytes, oligodendrocytes and microglia. Studies in vivo and in in vitro models have highlighted that the contribution of non-neuronal cells to the disease is a primary event and ALS pathogenesis is driven by both cell-autonomous and non-cell autonomous mechanisms. The advancements in genetics and in vitro modeling of the past 10 years have dramatically changed the way we investigate the pathogenic mechanisms involved in ALS. The identification of mutations in transactive response DNA-binding protein gene (TARDBP), fused in sarcoma (FUS) and, more recently, a GGGGCC-hexanucleotide repeat expansion in chromosome 9 open reading frame 72 (C9ORF72) and their link with familial ALS have provided new avenues of investigation and hypotheses on the pathophysiology of this devastating disease. In the same years, from 2007 to present, in vitro technologies to model neurological disorders have also undergone impressive developments. The advent of induced pluripotent stem cells (iPSCs) gave the field of ALS the opportunity to finally model in vitro not only familial, but also the larger part of ALS cases affected by sporadic disease. Since 2008, when the first human iPS-derived motor neurons from patients were cultured in a petri dish, several different techniques have been developed to produce iPSC lines through genetic reprogramming and multiple direct conversion methods have been optimised. In this review, we will give an overview of how human in vitro models have been used so far, what discoveries they have led to since 2007, and how the recent advances in technology combined with the genetic discoveries, have tremendously widened the horizon of ALS research.
肌萎缩侧索硬化症(ALS)是一种复杂的多因素疾病,其特征是运动神经元丧失,并累及其他几种细胞类型,包括星形胶质细胞、少突胶质细胞和小胶质细胞。体内和体外模型研究都强调,非神经元细胞对该疾病的影响是一个主要事件,ALS的发病机制是由细胞自主和非细胞自主机制共同驱动的。过去10年遗传学和体外建模方面的进展极大地改变了我们研究ALS致病机制的方式。转录激活反应DNA结合蛋白基因(TARDBP)、肉瘤融合基因(FUS)的突变,以及最近在9号染色体开放阅读框72(C9ORF72)中发现的GGGGCC六核苷酸重复扩增及其与家族性ALS的关联,为研究这种毁灭性疾病的病理生理学提供了新的研究途径和假设。在同一时期,从2007年至今,用于模拟神经疾病的体外技术也取得了令人瞩目的进展。诱导多能干细胞(iPSC)的出现使ALS领域终于有机会在体外不仅对家族性病例,而且对大部分散发性疾病影响的ALS病例进行建模。自2008年首例来自患者的人iPS衍生运动神经元在培养皿中培养以来,已经开发了几种不同的技术,通过基因重编程来产生iPSC系,并优化了多种直接转化方法。在这篇综述中,我们将概述迄今为止人类体外模型的使用情况、自2007年以来它们所带来的发现,以及技术上的最新进展与遗传学发现相结合如何极大地拓宽了ALS研究的视野。