ArticleNature communications2024
Mutant mice with rod-specific VPS35 deletion exhibit retinal α-synuclein pathology-associated degeneration.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Strategies for Optimizing Genetic Mouse Models to Enhance the Understanding of Parkinson's Disease.Biomedicines · 2026Review
- In vivo Proximity & Spatial Proteomics with CRISPR Screening Identify STXBP1 as a Protective Modifier of α-synuclein Toxicity in Dopamine Neurons.bioRxiv : the preprint server for biology · 2026Article
- Early retinal synaptic dysfunction and proteomic remodeling precede neurodegeneration in a Parkinson's disease model.NPJ Parkinson's disease · 2026Article
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- Advances in Optical Tissue Clearing for Three-Dimensional Ocular Imaging and Analysis.Journal of ophthalmology · 2026Review
- Recent Advances in Visual Dysfunction and Ocular Biomarkers in Neurological Disorders.Eye and brain · 2025Review
- Anesthetic effects on electrophysiological responses across the visual pathway.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Vacuolar protein sorting 35 (VPS35), the core component of the retromer complex which regulates endosomal trafficking, is genetically linked with Parkinson's disease (PD). Impaired vision is a common non-motor manifestation of PD. Here, we show mouse retinas with VPS35-deficient rods exhibit synapse loss and visual deficit, followed by progressive degeneration concomitant with the emergence of Lewy body-like inclusions and phospho-α-synuclein (P-αSyn) aggregation. Ultrastructural analyses reveal VPS35-deficient rods accumulate aggregates in late endosomes, deposited as lipofuscins bound to P-αSyn. Mechanistically, we uncover a protein network of VPS35 and its interaction with HSC70. VPS35 deficiency promotes sequestration of HSC70 and P-αSyn aggregation in late endosomes. Microglia which engulf lipofuscins and P-αSyn aggregates are activated, displaying autofluorescence, observed as bright dots in fundus imaging of live animals, coinciding with pathology onset and progression. The Rod
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