Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Neurosci Lett. 2021 Jun 11;755:135896. doi: 10.1016/j.neulet.2021.135896. Epub 2021 Apr 20.
Lysosomal free sialic acid storage disorder (FSASD) is an extremely rare, autosomal recessive, neurodegenerative, multisystemic disorder caused by defects in the lysosomal sialic acid membrane exporter SLC17A5 (sialin). SLC17A5 defects cause free sialic acid and some other acidic hexoses to accumulate in lysosomes, resulting in enlarged lysosomes in some cell types and 10-100-fold increased urinary excretion of free sialic acid. Clinical features of FSASD include coarse facial features, organomegaly, and progressive neurodegenerative symptoms with cognitive impairment, cerebellar ataxia and muscular hypotonia. Central hypomyelination with cerebellar atrophy and thinning of the corpus callosum are also prominent disease features. Around 200 FSASD cases are reported worldwide, with the clinical spectrum ranging from a severe infantile onset form, often lethal in early childhood, to a mild, less severe form with subjects living into adulthood, also called Salla disease. The pathobiology of FSASD remains poorly understood and FSASD is likely underdiagnosed. Known patients have experienced a diagnostic delay due to the rarity of the disorder, absence of routine urine sialic acid testing, and non-specific clinical symptoms, including developmental delay, ataxia and infantile hypomyelination. There is no approved therapy for FSASD. We initiated a multidisciplinary collaborative effort involving worldwide academic clinical and scientific FSASD experts, the National Institutes of Health (USA), and the FSASD patient advocacy group (Salla Treatment and Research [S.T.A.R.] Foundation) to overcome the scientific, clinical and financial challenges facing the development of new treatments for FSASD. We aim to collect data that incentivize industry to further develop, obtain approval for, and commercialize FSASD treatments. This review summarizes current aspects of FSASD diagnosis, prevalence, etiology, and disease models, as well as challenges on the path to therapeutic approaches for FSASD.
溶酶体游离唾液酸贮积症(FSASD)是一种极其罕见的常染色体隐性神经退行性多系统疾病,由溶酶体唾液酸膜输出蛋白 SLC17A5(唾液酸酶)缺陷引起。SLC17A5 缺陷导致游离唾液酸和其他一些酸性己糖在溶酶体中积累,导致一些细胞类型中的溶酶体增大,游离唾液酸的尿排泄增加 10-100 倍。FSASD 的临床特征包括粗面特征、器官肿大和进行性神经退行性症状,伴有认知障碍、小脑共济失调和肌肉张力减退。中枢性脑白质营养不良伴小脑萎缩和胼胝体变薄也是突出的疾病特征。全世界报道了约 200 例 FSASD 病例,其临床谱从严重的婴儿期发病形式(常于幼儿期内致死)到较轻、较不严重的形式(患者可存活至成年期,也称为 Salla 病)。FSASD 的病理生物学仍知之甚少,且该疾病可能诊断不足。由于疾病的罕见性、缺乏常规尿唾液酸检测以及非特异性临床症状(包括发育迟缓、共济失调和婴儿期脑白质营养不良),已知患者经历了诊断延迟。目前尚无 FSASD 的批准疗法。我们发起了一项多学科合作努力,涉及全球学术临床和科学 FSASD 专家、美国国立卫生研究院(NIH)和 FSASD 患者倡导组织(Salla 治疗与研究[S.T.A.R.]基金会),以克服为 FSASD 开发新疗法所面临的科学、临床和财务挑战。我们旨在收集数据,激励行业进一步开发、获得批准并商业化 FSASD 治疗方法。本综述总结了 FSASD 的诊断、患病率、病因和疾病模型的当前方面,以及在治疗方法的探索道路上面临的挑战。