ArticleeLife2024
Novel autophagy inducers by accelerating lysosomal clustering against Parkinson's disease.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Rebalancing α-Synuclein Clearance: Novel Therapeutic Frontiers in Parkinson's Disease.Neuromolecular medicine · 2026Review
- Glucocerebrosidase dysfunction in GBA1 carriers: insights from blood and macrophage analyses.Molecular biology reports · 2026Article
- Synthetic strategies for small molecule compounds for the treatment of Parkinson's disease: targeting α-synuclein.Molecular diversity · 2026Review
- HiExM Enables Scalable Mapping of Organelle Morphology and Spatial Heterogeneity.bioRxiv : the preprint server for biology · 2026Article
- Gaps in the Parkinson's disease therapeutic clinical pipeline: A focus on approaches targeting disease pathobiology.Journal of Parkinson's disease · 2026Review
- TIGAR Maintains Mitotic Spindle Organization and βII-Tubulin Stability in Glioma Stem Cells.CNS neuroscience & therapeutics · 2026Article
- DeepDrugDiscovery identifies blood-brain barrier permeable autophagy enhancers for Alzheimer's disease.Nature biomedical engineering · 2026Article
- Modest improvement of metabolic and behavioral deficits with long-term ambroxol treatment in a Pink1Acta pharmacologica Sinica · 2026Article
- Exploring Autophagy Inducing Molecules: Targeting Diverse Pathways in Alzheimer's Disease Management.Medicinal research reviews · 2026Review
- Research progress on the α-synuclein-lysosome axis in Parkinson's disease: molecular mechanisms of protein aggregation, autophagy dysfunction, and therapeutic targeting.Frontiers in neuroscience · 2026Review
- Systematic Characterization of LUHMES Cell-Based Parkinson's Disease Models Reveals Potential Novel Drug Targets.Molecular neurobiology · 2025Article
- LAMP2-FLOT2 interaction enhances autophagosome-lysosome fusion to protect the septic heart in response to ILC2.Autophagy · 2025Article
- R406 and its structural analogs reduce SNCA/α-synuclein levels via autophagic degradation.Autophagy · 2025Article
- Recent Advances in Autophagy and Immunotherapy for the Clearance of Aggregated α-Synuclein in Parkinson's Disease.Aging and disease · 2025Review
- Spatio-temporal processes in autophagosome-lysosome fusion.Medical review (2021) · 2025Review
- Synergistic Autophagy-Related Mechanisms of Protection Against Brain Aging and AD: Cellular Pathways and Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Clustering lysosomes around the MTOC: a promising strategy for SNCA/alpha-synuclein breakdown leading to parkinson disease treatment.Autophagy · 2024Article
- LAMTOR1 regulates dendritic lysosomal positioning in hippocampal neurons through TRPML1 inhibition.Frontiers in cellular neuroscience · 2024Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The autophagy-lysosome pathway plays an indispensable role in the protein quality control by degrading abnormal organelles and proteins including α-synuclein (αSyn) associated with the pathogenesis of Parkinson's disease (PD). However, the activation of this pathway is mainly by targeting lysosomal enzymic activity. Here, we focused on the autophagosome-lysosome fusion process around the microtubule-organizing center (MTOC) regulated by lysosomal positioning. Through high-throughput chemical screening, we identified 6 out of 1200 clinically approved drugs enabling the lysosomes to accumulate around the MTOC with autophagy flux enhancement. We further demonstrated that these compounds induce the lysosomal clustering through a JIP4-TRPML1-dependent mechanism. Among them, the lysosomal-clustering compound albendazole promoted the autophagy-dependent degradation of Triton-X-insoluble, proteasome inhibitor-induced aggregates. In a cellular PD model, albendazole boosted insoluble αSyn degradation. Our results revealed that lysosomal clustering can facilitate the breakdown of protein aggregates, suggesting that lysosome-clustering compounds may offer a promising therapeutic strategy against neurodegenerative diseases characterized by the presence of aggregate-prone proteins.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.