ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
α-Synuclein Pathology Spreads in a Midbrain-Hindbrain Assembloid Model.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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.
- Stem cell derived neural organoid approaches for neurological diseases.Neural regeneration research · 2026Article
- Advances in sex-specific single-cell transcriptomic profiling in Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Advances in neural organoids: structural organization, disease modeling, and applications in gene therapy.Molecular biology reports · 2026Review
- Next-Generation Strategies for Neural Repair and Regeneration: Neural Organoid Transplantation in the CNS.Cell proliferation · 2026Review
- Organoids in Cancer Research and Regenerative Medicine: Current Status, Challenges, and Future Prospects.MedComm · 2026Review
- Beyond Organ Boundaries: Molecular Mechanisms of Hepatic Encephalopathy and Parkinson's Disease from the Perspective of the Gut-Liver-Brain Axis.Research (Washington, D.C.) · 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
- Pluripotent stem cells-based neural organoids for modelling human brain development and diseases.Cell & bioscience · 2025Review
- Three-dimensional midbrain organoids: a next-generation tool for Parkinson's disease modelling and drug discovery.Stem cell research & therapy · 2025Review
- α-Synuclein Pathology Spreads in a Midbrain-Hindbrain Assembloid Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
15 authors.
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Abstract
Understanding the progression of α-synuclein pathology in neurodegenerative diseases such as Parkinson's disease (PD) is a longstanding challenge. Here, a novel midbrain-hindbrain-assembloid model that recapitulates the spread of α-synuclein pathology observed in PD patients, akin to Braak's hypothesis, is presented. Initially, the presence α-synuclein pathology is demonstrated in the hindbrain organoids. Subsequently, sophisticated tissue engineering methods are employed to create midbrain-hindbrain assembloids. These assembloids allow investigation and description of the spreading of α-synuclein pathology, as it progresses from the hindbrain components to the midbrain regions within the integrated structure. It is observed that an increase in α-synuclein in the hindbrain can induce transfer of the pathology into the healthy midbrain, as well as cause changes at the synapse level. The presented model constitutes a robust in vitro platform for investigating the mechanisms underlying α-synuclein spreading and disease progression, and holding potential for the screening of prospective therapeutics targeting the pathological propagation in PD and related synucleinopathies.
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