ArticleDisease models & mechanisms2019
Recapitulating Parkinson's disease pathology in a three-dimensional human neural cell culture model.
Article in Disease models & mechanisms, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Dopaminergic Identity of SH-SY5Y Cells Across Differentiation Protocols in Parkinson's Disease Research: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Research models to study lewy body dementia.Molecular neurodegeneration · 2025Review
- Modeling the neuroimmune system in Alzheimer's and Parkinson's diseases.Journal of neuroinflammation · 2024Review
- Electroconductive Collagen-Carbon Nanodots Nanocomposite Elicits Neurite Outgrowth, Supports Neurogenic Differentiation and Accelerates Electrophysiological Maturation of Neural Progenitor Spheroids.Advanced healthcare materials · 2024Article
- Advanced 3D Models of Human Brain Tissue Using Neural Cell Lines: State-of-the-Art and Future Prospects.Cells · 2023Review
- Susceptibility of Ovine Bone Marrow-Derived Mesenchymal Stem Cell Spheroids to Scrapie Prion Infection.Animals : an open access journal from MDPI · 2023Article
- Inflammation-Mediated Responses in the Development of Neurodegenerative Diseases.Advances in experimental medicine and biology · 2023Review
- Article
- Propagation of Parkinson's disease by extracellular vesicle production and secretion.Biochemical Society transactions · 2022Review
- Fiscalin Derivatives as Potential Neuroprotective Agents.Pharmaceutics · 2022Article
- Application and prospects of high-throughput screening forWorld journal of stem cells · 2022Review
- A Matrigel-based 3D construct of SH-SY5Y cells models the α-synuclein pathologies of Parkinson's disease.Disease models & mechanisms · 2022Article
- In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration.Nutrients · 2022Review
- Lipopeptide Pepducins as Therapeutic Agents.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Maternal pre-eclampsia serum increases neurite growth and mitochondrial function through a potential IL-6-dependent mechanism in differentiated SH-SY5Y cells.Frontiers in physiology · 2022Article
- Optimised techniques for high-throughput screening of differentiated SH-SY5Y cells and application for neurite outgrowth assays.Scientific reports · 2021Article
- HIV-1 Vpr protein impairs lysosome clearance causing SNCA/alpha-synuclein accumulation in neurons.Autophagy · 2021Article
- SHANK2 mutations impair apoptosis, proliferation and neurite outgrowth during early neuronal differentiation in SH-SY5Y cells.Scientific reports · 2021Article
- Influence of serum concentration in retinoic acid and phorbol ester induced differentiation of SH-SY5Y human neuroblastoma cell line.Molecular biology reports · 2020Article
- Alleviating toxic α-Synuclein accumulation by membrane depolarization: evidence from an in vitro model of Parkinson's disease.Molecular brain · 2020Article
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5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extensive loss of dopaminergic neurons and aggregation of the protein α-synuclein into ubiquitin-positive Lewy bodies represents a major neuropathological hallmark of Parkinson's disease (PD). At present, the generation of large nuclear-associated Lewy bodies from endogenous wild-type α-synuclein, translationally regulated under its own promoter in human cell culture models, requires costly and time-consuming protocols. Here, we demonstrate that fully differentiated human SH-SY5Y neuroblastoma cells grown in three-dimensional cell culture develop Lewy-body-like pathology upon exposure to exogenous α-synuclein species. In contrast to most cell- and rodent-based PD models, which exhibit multiple diffuse α-synuclein aggregates throughout the cytoplasm, a single large nuclear inclusion that is immunopositive for α-synuclein and ubiquitin is rapidly obtained in our model. This was achieved without the need for overexpression of α-synuclein or genetic modification of the cell line. However, phosphorylation of α-synuclein within these inclusions was not observed. The system described here provides an ideal tool to screen compounds to therapeutically intervene in Lewy body formation, and to investigate the mechanisms involved in disease progression in synucleinopathies.
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