MiR206 and 423-3p Are Differently Modulated in Fast and Slow-Progressing Amyotrophic Lateral Sclerosis Patients.

IF 3.3 4区 医学 Q2 NEUROSCIENCES NeuroMolecular Medicine Pub Date : 2024-03-15 DOI:10.1007/s12017-024-08773-6
Antonio Musarò, Gabriella Dobrowolny, Chiara Cambieri, Laura Libonati, Federica Moret, Irene Casola, Gaia Laurenzi, Matteo Garibaldi, Maurizio Inghilleri, Marco Ceccanti
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Abstract

Amyotrophic lateral sclerosis (ALS) is a rare neuromuscular disease with a wide disease progression. Despite several efforts to develop efficient biomarkers, many concerns about the available ones still need to be addressed. MicroRNA (miR) are non-coding RNAs that can modulate molecular circuits and are involved in ALS pathogenic mechanisms. 22 fast and 23 slow-progressing-defined ALS patients were recruited. ALSFRS-R, strength, respiratory function, nerve conduction studies, and creatine kinase were evaluated at the baseline and after 6 months of follow-up. The mean monthly reduction of the previous variables (progression index - PI) was calculated. MiR206, 133a-3p, 151a-5p, 199a-5p, and 423-3p were dosed. The univariate analysis showed an independent reduction of miR206 and an increase of miR423-3p in patients with a slow slope of ALSFRS-R and weakness, respectively. MiR206 and 423-3p are differently modulated in fast and slow-progressing ALS patients, suggesting a role for microRNAs in prognosis and therapeutic target.

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MiR206和423-3p在肌萎缩侧索硬化症快速进展期和缓慢进展期患者中的调制方式不同
肌萎缩性脊髓侧索硬化症(ALS)是一种罕见的神经肌肉疾病,疾病进展广泛。尽管为开发有效的生物标记物做出了许多努力,但现有的生物标记物仍有许多问题需要解决。微小核糖核酸(miR)是一种非编码 RNA,可调节分子回路,并参与 ALS 的致病机制。研究人员招募了 22 名快速进展和 23 名缓慢进展定义的 ALS 患者。在基线和随访 6 个月后对 ALSFRS-R、力量、呼吸功能、神经传导研究和肌酸激酶进行了评估。计算了前述变量的平均每月减少量(进展指数 - PI)。MiR206、133a-3p、151a-5p、199a-5p 和 423-3p 均有剂量。单变量分析显示,在 ALSFRS-R 和乏力斜率缓慢的患者中,miR206 和 miR423-3p 分别独立减少和增加。MiR206和423-3p在进展快和进展慢的ALS患者中的调节作用不同,这表明microRNA在预后和治疗目标中的作用不同。
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来源期刊
NeuroMolecular Medicine
NeuroMolecular Medicine 医学-神经科学
CiteScore
7.10
自引率
0.00%
发文量
33
审稿时长
>12 weeks
期刊介绍: NeuroMolecular Medicine publishes cutting-edge original research articles and critical reviews on the molecular and biochemical basis of neurological disorders. Studies range from genetic analyses of human populations to animal and cell culture models of neurological disorders. Emerging findings concerning the identification of genetic aberrancies and their pathogenic mechanisms at the molecular and cellular levels will be included. Also covered are experimental analyses of molecular cascades involved in the development and adult plasticity of the nervous system, in neurological dysfunction, and in neuronal degeneration and repair. NeuroMolecular Medicine encompasses basic research in the fields of molecular genetics, signal transduction, plasticity, and cell death. The information published in NEMM will provide a window into the future of molecular medicine for the nervous system.
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