Vinceti Marco, Urbano Teresa, Filippini Tommaso, Bedin Roberta, Simonini Cecilia, Sorarù Gianni, Trojsi Francesca, Michalke Bernhard, Mandrioli Jessica
CREAGEN - Environmental, Genetic, and Nutritional Epidemiology Research Center, Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy.
Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA.
Biol Trace Elem Res. 2025 Apr;203(4):2355-2364. doi: 10.1007/s12011-024-04311-4. Epub 2024 Jul 17.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting the brain and spinal cord motor neurons. On 25 April 2023, the drug tofersen, an antisense oligonucleotide, received the US Food and Drug Administration approval for treating ALS in adults carrying mutations of the SOD1 gene. We aimed at assessing whether cerebrospinal fluid concentrations of selenium, an element of both toxicological and nutritional interest possibly involved in disease etiology and progression, are modified by tofersen administration. We determined concentrations of selenium species by anion exchange chromatography hyphenated to inductively coupled plasma-dynamic reaction cell-mass spectrometry and overall selenium by using inductively coupled plasma sector-field mass spectrometry, at baseline and 6 months after active tofersen treatment in ten Italian ALS patients carrying the SOD1 gene mutation. Concentrations of total selenium and many selenium species substantially increased after the intervention, particularly of inorganic (tetravalent and hexavalent) selenium and of the organic species selenomethionine and a compound co-eluting with the selenocystine standard. Overall, these findings suggest that tofersen treatment markedly alters selenium status and probably the redox status within the central nervous system, possibly due to a direct effect on neurons and/or the blood-brain barrier. Further studies are required to investigate the biological and clinical relevance of these findings and how they might relate to the pharmacological effects of the drug and to disease progression.
肌萎缩侧索硬化症(ALS)是一种影响大脑和脊髓运动神经元的致命性神经退行性疾病。2023年4月25日,反义寡核苷酸药物托法替布获得美国食品药品监督管理局批准,用于治疗携带SOD1基因突变的成年ALS患者。我们旨在评估托法替布给药是否会改变脑脊液中硒的浓度,硒是一种在毒理学和营养学方面都备受关注的元素,可能与疾病的病因和进展有关。我们采用阴离子交换色谱与电感耦合等离子体-动态反应池-质谱联用技术测定硒物种的浓度,并使用电感耦合等离子体扇形磁场质谱法测定总硒浓度,对10名携带SOD1基因突变的意大利ALS患者在基线期以及接受托法替布积极治疗6个月后进行检测。干预后,总硒和许多硒物种的浓度大幅增加,尤其是无机(四价和六价)硒、有机物种硒代蛋氨酸以及一种与硒代胱氨酸标准品共洗脱的化合物。总体而言,这些发现表明托法替布治疗显著改变了中枢神经系统内的硒状态以及可能的氧化还原状态,这可能是由于对神经元和/或血脑屏障的直接作用所致。需要进一步研究来探讨这些发现的生物学和临床相关性,以及它们与药物的药理作用和疾病进展之间的关系。