Experimental Neuropathology Unit, Institute of Experimental Neurology (INSPE), Division of Neuroscience, San Raffaele Scientific Institute, 20132 Milan, Italy.
Laboratory of Clinical Molecular Biology, Unit of Genomics for human disease diagnosis, Division of Genetics and Cell Biology, San Raffaele Scientific Institute, 20132 Milan, Italy.
Int J Mol Sci. 2020 May 8;21(9):3346. doi: 10.3390/ijms21093346.
Although the genetic architecture of amyotrophic lateral sclerosis (ALS) is incompletely understood, recent findings suggest a complex model of inheritance in ALS, which is consistent with a multistep pathogenetic process. Therefore, the aim of our work is to further explore the architecture of ALS using targeted next generation sequencing (NGS) analysis, enriched in motor neuron diseases (MND)-associated genes which are also implicated in axonal hereditary motor neuropathy (HMN), in order to investigate if disease expression, including the progression rate, could be influenced by the combination of multiple rare gene variants. We analyzed 29 genes in an Italian cohort of 83 patients with both familial and sporadic ALS. Overall, we detected 43 rare variants in 17 different genes and found that 43.4% of the ALS patients harbored a variant in at least one of the investigated genes. Of note, 27.9% of the variants were identified in other MND- and HMN-associated genes. Moreover, multiple gene variants were identified in 17% of the patients. The burden of rare variants is associated with reduced survival and with the time to reach King stage 4, i.e., the time to reach the need for percutaneous endoscopic gastrostomy (PEG) positioning or non-invasive mechanical ventilation (NIMV) initiation, independently of known negative prognostic factors. Our data contribute to a better understanding of the molecular basis of ALS supporting the hypothesis that rare variant burden could play a role in the multistep model of disease and could exert a negative prognostic effect. Moreover, we further extend the genetic landscape of ALS to other MND-associated genes traditionally implicated in degenerative diseases of peripheral axons, such as HMN and CMT2.
虽然肌萎缩侧索硬化症(ALS)的遗传结构尚不完全清楚,但最近的研究结果表明,ALS 的遗传具有复杂的模式,与多步骤的发病机制一致。因此,我们的工作旨在使用靶向下一代测序(NGS)分析进一步探索 ALS 的结构,该分析富集了与运动神经元疾病(MND)相关的基因,这些基因也与遗传性运动神经病(HMN)的轴突有关,以研究疾病的表达,包括进展速度,是否可以受到多种罕见基因变异的组合的影响。我们分析了 83 名意大利家族性和散发性 ALS 患者的 29 个基因。总体而言,我们在 17 个不同的基因中检测到 43 个罕见变异,并发现 43.4%的 ALS 患者至少在一个研究基因中携带变异。值得注意的是,27.9%的变异存在于其他 MND 和 HMN 相关基因中。此外,17%的患者存在多种基因变异。罕见变异的负担与生存时间缩短以及达到 King 分期 4 有关,即需要进行经皮内镜胃造口术(PEG)定位或非侵入性机械通气(NIMV)的时间,与已知的负预后因素无关。我们的数据有助于更好地理解 ALS 的分子基础,支持罕见变异负担可能在疾病的多步骤模型中发挥作用并产生负预后影响的假设。此外,我们进一步将 ALS 的遗传图谱扩展到其他传统上与外周轴突退行性疾病相关的 MND 相关基因,如 HMN 和 CMT2。