ArticleMolecular brain2020
Endosomal dysfunction in iPSC-derived neural cells from Parkinson's disease patients with VPS35 D620N.
Article in Molecular brain, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Tracking Genetic Parkinson's Disease with Molecular Imaging: A Systematic Review.Movement disorders clinical practice · 2026Review
- Article
- Stem Cell-Based Approaches in Parkinson's Disease Research.International journal of stem cells · 2025Review
- Experimental Cell Models for Investigating Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Strategies for modeling aging and age-related diseases.npj aging · 2024Review
- VPS35 and retromer dysfunction in Parkinson's disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- The impact of VPS35 D620N mutation on alternative autophagy and its reversal by estrogen in Parkinson's disease.Cellular and molecular life sciences : CMLS · 2024Article
- Mitochondrial membrane proteins and VPS35 orchestrate selective removal of mtDNA.Nature communications · 2022Article
- Induced pluripotent stem cells: a tool for modeling Parkinson's disease.Trends in neurosciences · 2022Review
- Beware of Misdelivery: Multifaceted Role of Retromer Transport in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
- The Future of Genetic Disease Studies: Assembling an Updated Multidisciplinary Toolbox.Frontiers in cell and developmental biology · 2022Article
- Mitochondria and Other Organelles in Neural Development and Their Potential as Therapeutic Targets in Neurodegenerative Diseases.Frontiers in neuroscience · 2022Review
- Retromer dependent changes in cellular homeostasis and Parkinson's disease.Essays in biochemistry · 2021Review
- Review
- VPS35 Downregulation Alters Degradation Pathways in Neuronal Cells.Journal of Alzheimer's disease : JAD · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the Vacuolar protein sorting 35 (VPS35) gene have been linked to familial Parkinson's disease (PD), PARK17. VPS35 is a key component of the retromer complex, which plays a central role in endosomal trafficking. However, whether and how VPS35 deficiency or mutation contributes to PD pathogenesis remain unclear. Here, we analyzed human induced pluripotent stem cell (iPSC)-derived neurons from PD patients with the VPS35 D620N mutation and addressed relevant disease mechanisms. In the disease group, dopaminergic (DA) neurons underwent extensive apoptotic cell death. The movement of Rab5a- or Rab7a-positive endosomes was slower, and the endosome fission and fusion frequencies were lower in the PD group than in the healthy control group. Interestingly, vesicles positive for cation-independent mannose 6-phosphate receptor transported by retromers were abnormally localized in glial cells derived from patient iPSCs. Furthermore, we found α-synuclein accumulation in TH positive DA neurons. Our results demonstrate the induction of cell death, endosomal dysfunction and α -synuclein accumulation in neural cells of the PD group. PARK17 patient-derived iPSCs provide an excellent experimental tool for understanding the pathophysiology underlying PD.
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Registered trials
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