De Riso Giulia, Naef Valentina, Damiani Devid, Doccini Stefano, Santorelli Filippo M, Galatolo Daniele
Department of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, Naples, Italy.
A.O.U. Federico II, via Sergio Pansini 5, Naples, 80131, Italy.
Cerebellum. 2025 Jan 24;24(2):36. doi: 10.1007/s12311-025-01791-5.
Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a rare inherited condition described worldwide and characterized by a wide spectrum of heterogeneity in terms of genotype and phenotype. How sacsin loss leads to neurodegeneration is still unclear, and current knowledge indicates that sacsin is involved in multiple functional mechanisms. We hence hypothesized the existence of epigenetic factors, in particular alterations in methylation patterns, that could contribute to ARSACS pathogenesis and explain the pleiotropic effects of SACS further than pathogenic mutations. To investigate this issue, we recruited eight patients affected by ARSACS, four characterized by early onset of the disease and four with late onset. We performed Whole Genome Bisulfite Sequencing using DNA from peripheral blood to define the methylome of patients and compared them with a control group. Our analysis showed that patients with ARSACS exhibit an altered methylation pattern and that the observed differences exist also among affected individuals with different age of onset. Our study provides valuable insights for employing epigenetic biomarkers to assess the severity and progression of this disorder and propels further investigations into the role of epigenetic processes in ARSACS pathogenesis.
夏尔沃 - 萨格奈常染色体隐性痉挛性共济失调(ARSACS)是一种在全球范围内被描述的罕见遗传性疾病,其基因型和表型具有广泛的异质性。sacsin缺失如何导致神经退行性变仍不清楚,目前的知识表明sacsin参与多种功能机制。因此,我们推测存在表观遗传因素,特别是甲基化模式的改变,这可能导致ARSACS发病机制,并比致病突变更能解释SACS的多效性作用。为了研究这个问题,我们招募了8名受ARSACS影响的患者,其中4名疾病早发,4名晚发。我们使用外周血DNA进行全基因组亚硫酸氢盐测序来确定患者的甲基化组,并将其与对照组进行比较。我们的分析表明,ARSACS患者表现出甲基化模式改变,并且在不同发病年龄的受影响个体之间也存在观察到的差异。我们的研究为使用表观遗传生物标志物评估这种疾病的严重程度和进展提供了有价值的见解,并推动了对表观遗传过程在ARSACS发病机制中作用的进一步研究。