ArticleScience advances2022
Neuronal hyperactivity-induced oxidant stress promotes in vivo α-synuclein brain spreading.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Chronic Pain.Brain sciences · 2026Review
- Novel Non-Invasive PET Imaging of Reactive Oxygen Species Using [18 F]ROStrace in Three Proteinopathy-Associated Neurodegenerative Mouse Models.Academic radiology · 2026Article
- Membrane interfacial potential governs surface condensation and fibrillation of α-Synuclein in neurons.Nature communications · 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
- Short-Chain Fatty Acids Enhance EAAT2-Mediated Glutamate Clearance and Alleviate Oxidative Stress in an MPTP Mouse Model of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2025Article
- Stra8 links neuronal activity to inhibitory circuit protection in the adult mouse brain.Cell reports · 2025Article
- CHCHD2 mutant mice link mitochondrial deficits to PD pathophysiology.Science advances · 2025Article
- Chronic hyperactivation of midbrain dopamine neurons causes preferential dopamine neuron degeneration.eLife · 2025Article
- Protein Misfolding and Aggregation as a Mechanistic Link Between Chronic Pain and Neurodegenerative Diseases.Current issues in molecular biology · 2025Review
- Mitochondrial oxidant stress promotes α-synuclein aggregation and spreading in mice with mutated glucocerebrosidase.NPJ Parkinson's disease · 2024Article
- Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.International journal of molecular sciences · 2024Review
- Review
- The 'α-synucleinopathy syndicate': multiple system atrophy and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Current trends in basic research on Parkinson's disease: from mitochondria, lysosome to α-synuclein.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Positron Emission Tomography with [International journal of molecular sciences · 2024Article
- Evidence of compensatory neural hyperactivity in a subgroup of chemotherapy-treated breast cancer survivors and its association with brain aging.medRxiv : the preprint server for health sciences · 2024Article
- Molecular crosstalk between circadian clock and NLRP3 inflammasome signaling in Parkinson's disease.Heliyon · 2024Review
- The AAV-α-Synuclein Model of Parkinson's Disease: An Update.Journal of Parkinson's disease · 2024Review
- Evidence of compensatory neural hyperactivity in a subgroup of breast cancer survivors treated with chemotherapy and its association with brain aging.Frontiers in aging neuroscience · 2024Article
- Chronic stress hinders sensory axon regeneration via impairing mitochondrial cristae and OXPHOS.Science advances · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interneuronal transfer and brain spreading of pathogenic proteins are features of neurodegenerative diseases. Pathophysiological conditions and mechanisms affecting this spreading remain poorly understood. This study investigated the relationship between neuronal activity and interneuronal transfer of α-synuclein, a Parkinson-associated protein, and elucidated mechanisms underlying this relationship. In a mouse model of α-synuclein brain spreading, hyperactivity augmented and hypoactivity attenuated protein transfer. Important features of neuronal hyperactivity reported here were an exacerbation of oxidative and nitrative reactions, pronounced accumulation of nitrated α-synuclein, and increased protein aggregation. Data also pointed to mitochondria as key targets and likely sources of reactive oxygen and nitrogen species within hyperactive neurons. Rescue experiments designed to counteract the increased burden of reactive oxygen species reversed hyperactivity-induced α-synuclein nitration, aggregation, and interneuronal transfer, providing first evidence of a causal link between these pathological effects of neuronal stimulation and indicating a mechanistic role of oxidant stress in hyperactivity-induced α-synuclein spreading.
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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.