ArticleExperimental & molecular medicine2022
Inflammation promotes synucleinopathy propagation.
Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Post-Traumatic Stress Disorder and Risk of Degenerative Synucleinopathies: Systematic Review and Meta-Analysis.The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry · 2023Pooled it
- Neuroinflammation in neurodegenerative diseases: pathogenic pathways and emerging pharmacotherapeutic targets in Alzheimer's and Parkinson's disease.Inflammopharmacology · 2026Review
- α-Synuclein aggregates induce mitochondrial damage and trigger innate immunity to drive neuron-microglia communication.Nature communications · 2026Article
- Allergic disease as a risk factor for Parkinson's disease: a possible role of eosinophil.NPJ Parkinson's disease · 2026Article
- Lysophospholipids in Synucleinopathies: A Conceptual Framework Linking Proteostasis and Neuroinflammatory Signaling.Brain sciences · 2026Review
- Osmotin-derived 9-amino-acid peptide alleviates α-synuclein and MPTP-induced glial cell activation mediated neuroinflammation, protecting dopaminergic neurons in Parkinson's disease mice brain.Journal of biomedical science · 2026Article
- Spatial single-cell multiomics reveals peripheral immune dysfunction in Parkinson's and inflammatory bowel disease.NPJ Parkinson's disease · 2026Article
- Proteomic signatures of COVID-19 Post-Vaccination/Post-Infection Syndrome (PV/PIS): insights into immune dysregulation and coagulopathy.Frontiers in cellular and infection microbiology · 2026Article
- Disrupting α-Synuclein-ClpP interaction restores mitochondrial function and attenuates neuropathology in Parkinson's disease models.Molecular neurodegeneration · 2025Article
- Development and immunogenicity of adenoviral Fc-fused FMDV virus-like particle vaccine in swine.The veterinary quarterly · 2025Article
- White Blood Cells in Neurodegenerative Diseases in the Context of Neuroinflammation.Molecular neurobiology · 2025Review
- Potential Therapeutic Effects of Astragaloside IV in Parkinson's Disease Models via Modulation of α-syn-γH2AX-STING-IFN-I Axis.Molecular neurobiology · 2025Article
- Discovery of Blood-Based Proteins That Mark Benzo[a]pyrene Modulation of Autoimmunity.International journal of molecular sciences · 2025Article
- Serotype and distribution of adhesion genes in Streptococcus mutans isolated from people with Parkinson's disease.Odontology · 2025Article
- Applications of Limonene in Neoplasms and Non-Neoplastic Diseases.International journal of molecular sciences · 2025Review
- The Emerging Role of the Molecular Chaperone Clusterin in Parkinson's Disease.International journal of molecular sciences · 2025Review
- Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson's disease.Nature communications · 2025Article
- Microglia-driven inflammation induces progressive tauopathies and synucleinopathies.Experimental & molecular medicine · 2025Article
- Chemical Profiling and Assessment of Analgesic and Anti-Inflammatory Activity ofPharmaceuticals (Basel, Switzerland) · 2025Article
- The role of microglia in the prion-like transmission of protein aggregates in neurodegeneration.Brain communications · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The clinical progression of neurodegenerative diseases correlates with the spread of proteinopathy in the brain. The current understanding of the mechanism of proteinopathy spread is far from complete. Here, we propose that inflammation is fundamental to proteinopathy spread. A sequence variant of α-synuclein (V40G) was much less capable of fibril formation than wild-type α-synuclein (WT-syn) and, when mixed with WT-syn, interfered with its fibrillation. However, when V40G was injected intracerebrally into mice, it induced aggregate spreading even more effectively than WT-syn. Aggregate spreading was preceded by sustained microgliosis and inflammatory responses, which were more robust with V40G than with WT-syn. Oral administration of an anti-inflammatory agent suppressed aggregate spreading, inflammation, and behavioral deficits in mice. Furthermore, exposure of cells to inflammatory cytokines increased the cell-to-cell propagation of α-synuclein. These results suggest that the inflammatory microenvironment is the major driver of the spread of synucleinopathy in the brain.
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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.