Asbreuk Marije A B C, Schoenmakers Daphne H, Adang Laura Ann, Beerepoot Shanice, Bergner Caroline, Bley Annette, Boelens Jaap Jan, Bugiani Marianna, Calbi Valeria, García-Cazorla Àngeles, Eklund Erik A, Fumagalli Francesca, Grønborg Sabine Weller, Groeschel Samuel, Van Hasselt Peter M, Hollak Carla E M, Jones Simon A, de Koning Tom J, van Kuilenburg André B P, Laugwitz Lucia, Lindemans Caroline, Mochel Fanny, Øberg Andreas, Ram Dipak, Schöls Ludger, Sevin Caroline, Sinha Jigyasha, Vaz Frédéric M, Zerem Ayelet, Wolf Nicole I
Department of Child Neurology, Emma's Children's Hospital, Amsterdam UMC location Vrije Universiteit, the Netherlands.
Amsterdam Leukodystrophy Center, Amsterdam Neuroscience, Cellular & Molecular Mechanisms, the Netherlands.
Neurology. 2025 Jul 22;105(2):e213817. doi: 10.1212/WNL.0000000000213817. Epub 2025 Jun 27.
Metachromatic leukodystrophy (MLD) is a rare autosomal recessive lysosomal storage disorder caused by disease-causing variants in the gene coding for arylsulfatase A, leading to deficient enzyme activity and subsequent accumulation of sulfatides. MLD is characterized by demyelination and neurodegeneration of the central and peripheral nervous system, manifesting as progressive motor and cognitive defects in affected individuals. This review provides a comprehensive overview of the significant progress made in MLD research in the past decade, regarding natural history, disease and treatment mechanisms, and newborn screening (NBS). Traditionally, MLD has been classified according to age at onset (late-infantile, early-juvenile and late-juvenile, and adult MLD), with earlier forms leading to more rapid neurologic decline. New data show that the type of presenting symptoms further influences the dynamic of disease progression. Patients with a cognitive presentation have a much slower or even no motor decline than patients with a mixed motor and cognitive presentation. Research advancements have enabled improved understanding of the effects of allogeneic hematopoietic stem cell transplantation and the development of novel therapeutic approaches, including hematopoietic stem cell gene therapy, which is now authorized in the EU, United Kingdom, and United States as treatment for selected patients with early-onset forms of MLD. Both hematopoietic stem cell transplantation and hematopoietic stem cell gene therapy are most effective when administered before disease onset. To identify presymptomatic patients, NBS for MLD is becoming available in several countries, resulting in new challenges. Decisions regarding patient eligibility for these treatments in already symptomatic individuals, as well as the timing of treatment for patients identified through NBS, require thorough understanding of disease progression. Biomarkers may be helpful for disease staging and prediction of disease evolution. Moreover, apart from timing, challenges remain regarding optimal treatment strategies across MLD subtypes, especially late-onset MLD, and management of the clinical heterogeneity and course of the disease. Another important issue is ensuring therapy accessibility, which forms a substantial barrier for equitable care. Continued research and international collaboration are essential to address these challenges, with the goal of improving care and outcomes for patients with MLD and their families.
异染性脑白质营养不良(MLD)是一种罕见的常染色体隐性溶酶体贮积症,由芳基硫酸酯酶A编码基因中的致病变异引起,导致酶活性缺乏,随后硫脂蓄积。MLD的特征是中枢和周围神经系统的脱髓鞘和神经变性,在受影响个体中表现为进行性运动和认知缺陷。本综述全面概述了过去十年MLD研究在自然史、疾病和治疗机制以及新生儿筛查(NBS)方面取得的重大进展。传统上,MLD根据发病年龄(晚婴儿型、早青少年型和晚青少年型以及成人MLD)进行分类,发病较早的类型导致神经功能衰退更快。新数据表明,出现的症状类型进一步影响疾病进展的动态。认知表现的患者比运动和认知混合表现的患者运动衰退要慢得多,甚至没有运动衰退。研究进展使人们对异基因造血干细胞移植的效果有了更好的理解,并推动了新治疗方法的发展,包括造血干细胞基因治疗,目前该疗法在欧盟、英国和美国已被批准用于治疗某些早发型MLD患者。造血干细胞移植和造血干细胞基因治疗在疾病发作前给药时最有效。为了识别无症状患者,可以在几个国家进行MLD的新生儿筛查,这带来了新的挑战。对于已经出现症状的个体,决定其是否适合这些治疗,以及对于通过新生儿筛查确定的患者的治疗时机,都需要深入了解疾病进展。生物标志物可能有助于疾病分期和疾病演变的预测。此外,除了时机问题,MLD各亚型的最佳治疗策略,尤其是晚发型MLD,以及疾病临床异质性和病程的管理仍然存在挑战。另一个重要问题是确保治疗的可及性,这是公平医疗的一个重大障碍。持续的研究和国际合作对于应对这些挑战至关重要,目标是改善MLD患者及其家庭的护理和治疗结果。