Department of Neuromuscular Disorders, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK.
J Neurol. 2021 Aug;268(8):3031-3041. doi: 10.1007/s00415-020-10218-6. Epub 2020 Oct 26.
Dentatorubral-pallidoluysian atrophy (DRPLA) is a rare neurodegenerative disorder caused by CAG repeat expansions in the atrophin-1 gene and is inherited in an autosomal dominant fashion. There are currently no disease-modifying treatments available. The broad development of therapies for DRPLA, as well as other similar rare diseases, has hit a roadblock due to the rarity of the condition and the wide global distribution of patients and families, consequently inhibiting biomarker development and therapeutic research. Considering the shifting focus towards diverse populations, widespread genetic testing, rapid advancements in the development of clinical and wet biomarkers for Huntington's disease (HD), and the ongoing clinical trials for antisense oligonucleotide (ASO) therapies, the prospect of developing effective treatments in rare disorders has completely changed. The awareness of the HD ASO program has prompted global collaboration for rare disorders in natural history studies and the development of biomarkers, with the eventual goal of undergoing treatment trials. Here, we discuss DRPLA, which shares similarities with HD, and how in this and other repeat expansion disorders, neurogenetics groups like ours at UCL are gearing up for forthcoming natural history studies to accelerate future ASO treatment trials to hopefully emulate the progress seen in HD.
齿状核红核苍白球路易体萎缩症(DRPLA)是一种由 atrophin-1 基因突变引起的罕见神经退行性疾病,呈常染色体显性遗传。目前尚无针对该病的治疗方法。由于该病的罕见性以及患者和家属在全球范围内的广泛分布,DRPLA 等其他类似罕见疾病的治疗方法的广泛开发遇到了障碍,从而抑制了生物标志物的开发和治疗研究。鉴于人们的关注焦点转向了不同人群、广泛的基因检测、亨廷顿病(HD)的临床和湿生物标志物的快速发展,以及针对反义寡核苷酸(ASO)疗法的临床试验正在进行,罕见疾病的有效治疗方法的前景已经发生了彻底改变。对 HD ASO 计划的认识促使全球合作开展罕见疾病的自然史研究和生物标志物的开发,最终目标是进行治疗试验。在这里,我们讨论了与 HD 具有相似之处的 DRPLA,以及在这种和其他重复扩展疾病中,像我们 UCL 这样的神经遗传学小组如何为即将到来的自然史研究做好准备,以加速未来的 ASO 治疗试验,希望能效仿在 HD 中看到的进展。