ArticleThe Journal of clinical investigation2019
Oxidative stress in vagal neurons promotes parkinsonian pathology and intercellular α-synuclein transfer.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
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Who cites it
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
- Neuroprotective Effects of Resveratrol in In vivo and In vitro Experimental Models of Parkinson's Disease: a Systematic Review.Neurotoxicity research · 2022Pooled it
- Chronic Paraquat Neurotoxicity and Dopaminergic Degeneration: A Mechanistic Review.Chemistry & biodiversity · 2026Review
- Hypoxia and TTR dysregulation in astrocytes from Parkinson's disease with a specific mitochondrial haplogroup: A single-cell analysis.Neural regeneration research · 2026Article
- Novel Non-Invasive PET Imaging of Reactive Oxygen Species Using [18 F]ROStrace in Three Proteinopathy-Associated Neurodegenerative Mouse Models.Academic radiology · 2026Article
- The Brain-Gut Axis in Parkinson's Disease Pathology.Comprehensive Physiology · 2026Review
- Untargeted serum metabolomics and air pollution in Parkinson's disease.Research square · 2026Article
- Selective peroxynitrite-mediated protein nitration catalyzed by glyoxalase domain containing protein 4.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Alpha-Synuclein Dynamics in Cerebral Ischemia.ASN neuro · 2026Review
- Organelle-Targeted Nanotherapeutics for Parkinson's Disease: From Pathogenesis to Preclinical Strategies and Translational Challenges.International journal of nanomedicine · 2026Review
- Propagation of α-synuclein pathology: models, mechanisms and future goals.Molecular neurodegeneration advances · 2026Review
- Therapeutic Potentials of the Seaweed-Derived Compounds for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2025Review
- Unraveling the Vicious Cycle: Oxidative Stress and Neurotoxicity in Neurodegenerative Diseases.FASEB bioAdvances · 2025Review
- Oxygen-induced stress reveals context-specific gene regulatory effects in human brain organoids.Genome research · 2025Article
- Alpha-synuclein seeding amplification assays in Lewy body dementia: a brief review.Molecular neurodegeneration · 2025Review
- The Potential Role of Oxidative Stress in Modulating Airway Defensive Reflexes.Antioxidants (Basel, Switzerland) · 2025Review
- Fasudil inhibits α-synuclein aggregation through ROCK-inhibition-mediated mechanisms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Oxidative stress and dysregulated long noncoding RNAs in the pathogenesis of Parkinson's disease.Biological research · 2025Review
- Peripheral proteinopathy in neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Seed Amplification Assays as Powerful Tools for Detecting Peripheral Biomarkers in Prion-Like Diseases.Sub-cellular biochemistry · 2025Review
- Mitochondrial oxidant stress promotes α-synuclein aggregation and spreading in mice with mutated glucocerebrosidase.NPJ Parkinson's disease · 2024Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Specific neuronal populations display high vulnerability to pathological processes in Parkinson's disease (PD). The dorsal motor nucleus of the vagus nerve (DMnX) is a primary site of pathological α-synuclein deposition and may play a key role in the spreading of α-synuclein lesions within and outside the CNS. Using in vivo models, we show that cholinergic neurons forming this nucleus are particularly susceptible to oxidative challenges and accumulation of reactive oxidative species (ROS). Targeted α-synuclein overexpression within these neurons triggered an oxidative stress that became significantly more pronounced after exposure to the ROS-generating agent paraquat. A more severe oxidative stress resulted in enhanced production of oxidatively modified forms of α-synuclein, increased α-synuclein aggregation into oligomeric species and marked degeneration of DMnX neurons. Enhanced oxidative stress also affected neuron-to-neuron protein transfer, causing an increased spreading of α-synuclein from the DMnX toward more rostral brain regions. In vitro experiments confirmed a greater propensity of α-synuclein to pass from cell to cell under pro-oxidant conditions, and identified nitrated α-synuclein forms as highly transferable protein species. These findings substantiate the relevance of oxidative injury in PD pathogenetic processes, establish a relationship between oxidative stress and vulnerability to α-synuclein pathology and define a new mechanism, enhanced cell-to-cell α-synuclein transmission, by which oxidative stress could promote PD development and progression.
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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.