ArticleNPJ Parkinson's disease2023
Extracellular high molecular weight α-synuclein oligomers induce cell death by disrupting the plasma membrane.
Article in NPJ Parkinson's disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Cofilin 1-138 Promotes Mitochondrial Dysfunction and Synaptic Degeneration in Parkinson's Disease.Molecular neurobiology · 2026Article
- Insight into the Neuroprotective Mechanisms of Resveratrol: Inhibition of Alpha-Synuclein Fibrillation and its Role in Mitigating Toxicity.Cell biochemistry and biophysics · 2026Article
- Microengineering of the capillary interface of midbrain dopaminergic neurons to study Parkinson's disease vascular alterations.Communications engineering · 2026Article
- Microfluidic platform for understanding Parkinson's disease and α-synuclein conformation.Translational neurodegeneration · 2025Review
- Cellular prion protein and calcium ions trigger the neurotoxicity of α-synuclein aggregates.Cell & bioscience · 2025Article
- Unveiling Exosomes and Microvesicles in Parkinson's Disease: Mechanistic Insights Into Cell Death Pathways and Therapeutic Potential.Molecular neurobiology · 2025Review
- Abnormal α-synuclein binds to synaptotagmin 13, impairing extracellular vesicle release in synucleinopathies.Translational neurodegeneration · 2025Article
- Sulfate reducing bacteria induce α-synuclein in intestinal and neuronal cells and tissues and inhibit tyrosine hydroxylase in neuronal cells.Frontiers in neuroscience · 2025Article
- Alpha-synuclein aggregation induces prominent cellular lipid changes as revealed by Raman spectroscopy and machine learning analysis.Brain communications · 2025Article
- Current insights and assumptions on α-synuclein in Lewy body disease.Acta neuropathologica · 2024Review
- Plasminogen degrades α-synuclein, Tau and TDP-43 and decreases dopaminergic neurodegeneration in mouse models of Parkinson's disease.Scientific reports · 2024Article
- Cell biology of Parkinson's disease: Mechanisms of synaptic, lysosomal, and mitochondrial dysfunction.Current opinion in neurobiology · 2024Review
- New views on the complex interplay between degeneration and autoimmunity in multiple sclerosis.Frontiers in cellular neuroscience · 2024Article
- Alpha-Synuclein Contribution to Neuronal and Glial Damage in Parkinson's Disease.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
α-Synuclein (αS), the causative protein of Parkinson's disease and other α-synucleinopathies, aggregates from a low molecular weight form (LMW-αS) to a high molecular weight αS oligomer (HMW-αSo). Aggregated αS accumulates intracellularly, induces intrinsic apoptosis, is released extracellularly, and appears to propagate disease through prion-like spreading. Whether extracellular αS aggregates are cytotoxic, damage cell wall, or induce cell death is unclear. We investigated cytotoxicity and cell death caused by HMW-αSo or LMW-αS. Extracellular HMW-αSo was more cytotoxic than LMW-αS and was a crucial factor for inducing plasma membrane damage and cell death. HMW-αSo induced reactive oxygen species production and phospholipid peroxidation in the membrane, thereby impairing calcium homeostasis and disrupting plasma membrane integrity. HMW-αSo also induced extrinsic apoptosis and cell death by activating acidic sphingomyelinase. Thus, as extracellular HMW-αSo causes neuronal injury and death via cellular transmission and direct plasma membrane damage, we propose an additional disease progression pathway for α-synucleinopathies.
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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 OpenQuestion graph.