ArticlePloS one2013
Triggering of inflammasome by aggregated α-synuclein, an inflammatory response in synucleinopathies.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 349 papers.
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Who cites it
349 citing papers in PubMed, 573 citations in OpenAlex.
- Discovery of a brain penetrant NLRP3 inflammasome inhibitor that reduces neuropathic pain in mice.European journal of medicinal chemistry · 2026Article
- Pharmacological modulation of cGAS-STING-NLRP3 signaling by nano-immunomodulators in Alzheimer and Parkinson disease.Inflammopharmacology · 2026Review
- Unraveling Neurodegeneration: Common Molecular Mechanisms and Novel Therapeutic Concepts in Major Neurodegenerative Disorders.Brain and behavior · 2026Review
- Article
- Brain-muscle axis regulation of neuroinflammation and sarcopenia in Parkinson's disease: the bridging role of lactylation.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- Peripheral immunochemical considerations in Parkinson disease: sources, targets and crosstalk mechanisms.Journal of translational medicine · 2026Review
- PET-MRI biomarkers reveal efficacy of a novel NLRP3 inhibitor in Parkinson's disease models.Brain : a journal of neurology · 2026Article
- Repurposing Antidiabetic Medications for Parkinson's Disease: Focus on Biomarker Strategies for Disease Modification.International journal of molecular sciences · 2026Review
- Immunosenescence in Human Disease: Mechanistic Insights and Therapeutic Opportunities.Biomolecules & therapeutics · 2026Review
- Mitochondrial DNA: a molecular switch driving sterile neuroinflammation.Translational neurodegeneration · 2026Review
- Ester Prodrug NLRP3 Inflammasome Inhibitor NT-0796 is Brain Active due to Activation by Local Expression of Carboxylesterase-1.ACS chemical neuroscience · 2026Article
- C1q-dependent clearance of alpha-synuclein allows macrophages to transiently limit enteric synucleinopathy in male mice.Nature communications · 2026Article
- Neuroprotective effect of sinomenine on parkinson's disease through NLRP3/Caspase-1/GSDMD pathway-mediated pyroptosis inhibition.Metabolic brain disease · 2026Article
- Research progress on the α-synuclein-lysosome axis in Parkinson's disease: molecular mechanisms of protein aggregation, autophagy dysfunction, and therapeutic targeting.Frontiers in neuroscience · 2026Review
- MiR-7 in neurological disorders: beyond metabolic dysregulation.Frontiers in neuroscience · 2026Review
- Targeting Cathepsins in Neurodegeneration: Biochemical Advances.Biomedicines · 2025Review
- Sequelae of viral CNS infections including outcomes, mechanisms, and knowledge gaps.Npj viruses · 2025Review
- Th2 cell-derived exosomes alleviate central nervous system inflammation and demyelination in experimental autoimmune encephalomyelitis by regulating inflammasomes to inhibit microglia activation.Molecular biology reports · 2025Article
- Profile of NT-0527, a brain penetrant NLRP3 Inflammasome inhibitor suitable as anRSC medicinal chemistry · 2025Article
- IL-1 family cytokines in inflammation and immunity.Cellular & molecular immunology · 2025Review
289 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is one of the most common neurodegenerative diseases. It is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta of the brain. Another feature is represented by the formation in these cells of inclusions called Lewy bodies (LB), principally constituted by fibrillar α-synuclein (αSyn). This protein is considered a key element in the aetiology of a group of neurodegenerative disorders termed synucleinopathies, which include PD, but the cellular and molecular mechanisms involved are not completely clear. It is established that the inflammatory process plays a crucial role in the pathogenesis and/or progression of PD; moreover, it is known that aggregated αSyn, released by neurons, activates microglia cells to produce pro-inflammatory mediators, such as IL-1β. IL-1β is one of the strongest pro-inflammatory cytokines; it is produced as an inactive mediator, and its maturation and activation requires inflammasome activation. In particular, the NLRP3 inflammasome is activated by a wide variety of stimuli, among which are crystallized and particulate material. In this work, we investigated the possibility that IL-1β production, induced by fibrillar αSyn, is involved the inflammasome activation. We demonstrated the competence of monomeric and fibrillar αSyn to induce synthesis of IL-1β, through TLR2 interaction; we found that the secretion of the mature cytokine was a peculiarity of the fibrillated protein. Moreover, we observed that the secretion of IL-1β involves NLRP3 inflammasome activation. The latter relies on the phagocytosis of fibrillar αSyn, followed by increased ROS production and cathepsin B release into the cytosol. Taken together, our data support the notion that fibrillar αSyn, likely released by neuronal degeneration, acts as an endogenous trigger inducing a strong inflammatory response in PD.
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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.