Gardner Emily, Mole Sara E
MRC Laboratory for Molecular Cell Biology and Great Ormond Street Institute of Child Health, University College London, London, United Kingdom.
Front Neurol. 2021 Oct 18;12:754045. doi: 10.3389/fneur.2021.754045. eCollection 2021.
The neuronal ceroid lipofuscinoses (NCLs) are a group of inherited neurodegenerative disorders that affect children and adults. They share some similar clinical features and the accumulation of autofluorescent storage material. Since the discovery of the first causative genes, more than 530 mutations have been identified across 13 genes in cases diagnosed with NCL. These genes encode a variety of proteins whose functions have not been fully defined; most are lysosomal enzymes, or transmembrane proteins of the lysosome or other organelles. Many mutations in these genes are associated with a typical NCL disease phenotype. However, increasing numbers of variant disease phenotypes are being described, affecting age of onset, severity or progression, and including some distinct clinical phenotypes. This data is collated by the NCL Mutation Database which allows analysis from many perspectives. This article will summarise and interpret current knowledge and understanding of their genetic basis and phenotypic heterogeneity.
神经元蜡样脂褐质沉积症(NCLs)是一组影响儿童和成人的遗传性神经退行性疾病。它们具有一些相似的临床特征以及自体荧光储存物质的积累。自首个致病基因被发现以来,在被诊断为NCL的病例中,已在13个基因中鉴定出超过530种突变。这些基因编码多种功能尚未完全明确的蛋白质;大多数是溶酶体酶,或溶酶体或其他细胞器的跨膜蛋白。这些基因中的许多突变与典型的NCL疾病表型相关。然而,越来越多的变异疾病表型正在被描述,影响发病年龄、严重程度或进展情况,并且包括一些独特的临床表型。这些数据由NCL突变数据库整理,该数据库允许从多个角度进行分析。本文将总结并解释目前对其遗传基础和表型异质性的认识和理解。