Department of Neurology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Research Institute for Diseases of Old Age, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Brain. 2020 Apr 1;143(4):1190-1205. doi: 10.1093/brain/awaa064.
Recently, the genetic variability in lysosomal storage disorders has been implicated in the pathogenesis of Parkinson's disease. Here, we found that variants in prosaposin (PSAP), a rare causative gene of various types of lysosomal storage disorders, are linked to Parkinson's disease. Genetic mutation screening revealed three pathogenic mutations in the saposin D domain of PSAP from three families with autosomal dominant Parkinson's disease. Whole-exome sequencing revealed no other variants in previously identified Parkinson's disease-causing or lysosomal storage disorder-causing genes. A case-control association study found two variants in the intronic regions of the PSAP saposin D domain (rs4747203 and rs885828) in sporadic Parkinson's disease had significantly higher allele frequencies in a combined cohort of Japan and Taiwan. We found the abnormal accumulation of autophagic vacuoles, impaired autophagic flux, altered intracellular localization of prosaposin, and an aggregation of α-synuclein in patient-derived skin fibroblasts or induced pluripotent stem cell-derived dopaminergic neurons. In mice, a Psap saposin D mutation caused progressive motor decline and dopaminergic neurodegeneration. Our data provide novel genetic evidence for the involvement of the PSAP saposin D domain in Parkinson's disease.
最近,溶酶体贮积症的遗传变异性被认为与帕金森病的发病机制有关。在这里,我们发现了前蛋白(PSAP)的变异与帕金森病有关,前蛋白是各种类型溶酶体贮积症的罕见致病基因。遗传突变筛选显示,三个常染色体显性遗传帕金森病家系的 PSAP 中存在 saposin D 结构域的三个致病性突变。外显子组测序未发现先前确定的帕金森病致病基因或溶酶体贮积症致病基因的其他变异。病例对照关联研究发现,PSAP saposin D 结构域内含子区域的两个变异(rs4747203 和 rs885828)在日本和中国台湾的综合队列中散发性帕金森病的等位基因频率显著升高。我们发现,在患者来源的皮肤成纤维细胞或诱导多能干细胞衍生的多巴胺能神经元中,自噬小泡异常积累,自噬流受损,前蛋白的细胞内定位改变,α-突触核蛋白聚集。在小鼠中,Psap saposin D 突变导致进行性运动减退和多巴胺能神经退行性变。我们的数据为 PSAP saposin D 结构域参与帕金森病提供了新的遗传证据。