ArticleNPJ Parkinson's disease2025
A high-fidelity microfluidic platform reveals retrograde propagation as the main mechanism of α-Synuclein spread in human neurons.
Article in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Activated microglial phenotypes in the hippocampal CA2 subfield are implicated in Lewy body disease progression.Acta neuropathologica · 2026Article
- Modeling Parkinson's pathology in human iPSC dopaminergic neurons uncovers key mechanisms of Lewy body formation and heterogeneity.Science advances · 2026Article
- Microfluidic co-culture system for synaptically segregated neural networks to explore astrocyte-driven neural pathology.Microsystems & nanoengineering · 2026Article
- Axonal Transport Deficits in Parkinson's Disease: Insights from Neurotoxin, Genetic, and Sporadic Models.Brain sciences · 2026Review
- A Microfluidic Framework for Neuroprotective Compound Triage Across Ischemia and Neurodegeneration.Molecules (Basel, Switzerland) · 2026Review
- Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases.Translational neurodegeneration · 2026Review
- α-Synuclein in Lewy Body Diseases: Progress, Remaining Challenges and Future Perspectives.Expert reviews in molecular medicine · 2026Review
- Microglial reactivity in the hippocampal CA2 is associated with advanced neuronal α-synucleinopathy.bioRxiv : the preprint server for biology · 2026Article
- Propagation of α-synuclein pathology: models, mechanisms and future goals.Molecular neurodegeneration advances · 2026Review
- Development of convolutional neural networks for automated brain-wide histopathological analysis in mouse models of synucleinopathies.NPJ Parkinson's disease · 2025Article
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Authors and funding
10 authors.
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Abstract
α-Synuclein (αSyn) is a major component of Lewy bodies and Lewy neurites, which are a pathological hallmark of Parkinson's disease (PD). Pathologically aggregated forms of αSyn can spread along neurites and induce the misfolding of normal αSyn. To elucidate how αSyn pathology propagates between brain areas, we developed a novel in vitro microfluidic platform to study the intracellular transport of preformed fibrils and the induction and spread of αSyn aggregates. Patient-derived midbrain dopaminergic (mDA) neurons were cultured in microfluidic devices designed to maintain unidirectional axonal connections between fluidically isolated mDA neuronal cultures for over 3 months. Using αSyn preformed fibrils to induce Lewy-like pathology, we found that anterograde spread of αSyn fibrils was slow and occurred at low levels, while retrograde spread was significantly more efficient. This is in line with observations in animal models and shows that the platform provides an innovative new tool for studying PD in vitro.
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