| Literature DB >> 32201884 |
Yutaka Oji1, Taku Hatano1, Shin-Ichi Ueno1, Manabu Funayama2, Kei-Ichi Ishikawa1,3, Ayami Okuzumi1, Sachiko Noda1, Shigeto Sato1, Wataru Satake4, Tatsushi Toda4, Yuanzhe Li1, Tomoko Hino-Takai5, Soichiro Kakuta6, Taiji Tsunemi1, Hiroyo Yoshino2, Kenya Nishioka1, Tatsuya Hattori7, Yasuaki Mizutani8, Tatsuro Mutoh8, Fusako Yokochi9, Yuta Ichinose10, Kishin Koh10, Kazumasa Shindo10, Yoshihisa Takiyama10, Tsuyoshi Hamaguchi11, Masahito Yamada11, Matthew J Farrer12,13, Yasuo Uchiyama14, Wado Akamatsu3, Yih-Ru Wu15, Junko Matsuda5, Nobutaka Hattori1.
Abstract
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.Entities:
Keywords: Parkinson’s disease; lysosomal storage disorder; prosaposin; saposin D; α-synuclein
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Year: 2020 PMID: 32201884 DOI: 10.1093/brain/awaa064
Source DB: PubMed Journal: Brain ISSN: 0006-8950 Impact factor: 13.501