ReviewJournal of cell science2026
Clathrin-mediated endocytosis as an axis for the etiopathogenesis of Parkinson's disease.
Review in Journal of cell science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Clathrin-mediated endocytosis (CME) is a core process in eukaryotic cells, providing a mechanism to selectively take up cargo from the extracellular space into the cytoplasm. Emerging data from both Mendelian and idiopathic forms of Parkinson's disease and parkinsonism syndromes supports a role for key players in CME in determining the risk of developing these neurodegenerative disorders. This Perspective summarizes the current genetic and functional evidence supporting a role for CME in Parkinson's disease, suggesting routes through which CME dysfunction could contribute to the etiopathogenesis of this disorder, and discussing the therapeutic potential for targeting CME in the context of neurodegeneration linked to Parkinson's disease and parkinsonism.
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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.