ReviewFrontiers in molecular neuroscience2022
Crosstalk Between the NLRP3 Inflammasome/ASC Speck and Amyloid Protein Aggregates Drives Disease Progression in Alzheimer's and Parkinson's Disease.
Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 57 citations in OpenAlex.
- The ASC-c isoform as a modulator of inflammasome activation: Insights into molecular mechanisms and therapeutic applications.The Journal of biological chemistry · 2026Article
- Neuronal inflammasomes: balancing immunity, neuroinflammation, and homeostasis.Trends in immunology · 2026Review
- Constructing Curcumin-Based Biological Metal-Organic Frameworks (MOFs) for the Treatment of Alzheimer's Disease Through the Pyroptosis Pathway.International journal of molecular sciences · 2026Article
- Characterization of the Proteomic Response in SIM-A9 Murine Microglia Following Canonical NLRP3 Inflammasome Activation.International journal of molecular sciences · 2026Article
- Targeting microglia-mediated neuroinflammation in Alzheimer's disease: mechanisms and therapeutic approaches.Frontiers in immunology · 2026Review
- Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.Life (Basel, Switzerland) · 2025Review
- Neurometabolomic impacts of wood smoke and protective benefits of anti-aging therapeutics in aged female C57BL/6J mice.Particle and fibre toxicology · 2025Article
- Unlocking Therapeutic Potential of Novel Thieno-Oxazepine Hybrids as Multi-Target Inhibitors of AChE/BChE and Evaluation Against Alzheimer's Disease: In Vivo, In Vitro, Histopathological, and Docking Studies.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Role of Peripheral NLRP3 Inflammasome in Cognitive Impairments: Insights of Non-central Factors.Molecular neurobiology · 2025Review
- pS396/pS404 (PHF1) tau vaccine outperforms pS199/pS202 (AT8) in rTg4510 tauopathy model.NPJ vaccines · 2025Article
- IC100 blocks inflammasome activation induced by α-synuclein aggregates and ASC specks.NPJ Parkinson's disease · 2025Article
- Targeting of phosphorylated tau at threonine 181 by a Qβ virus-like particle vaccine is safe, highly immunogenic, and reduces disease severity in mice and rhesus macaques.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Targeting NLRP3 Inflammasomes: A Trojan Horse Strategy for Intervention in Neurological Disorders.Molecular neurobiology · 2025Review
- Inflammasomes in Alzheimer's Progression: Nrf2 as a Preventive Target.Antioxidants (Basel, Switzerland) · 2025Review
- Alleviating the NF-κB/NLRP3 pathway-mediated pyroptosis and ameliorating the cognitive function of aged mice post partial hepatectomy by increasing the Bmal1 level via subanesthetic doses of ketamine.Translational neuroscience · 2025Article
- Broad-spectrum inflammasome inhibition by thiomuscimol.Cell death discovery · 2024Article
- Review
- Mechanism of flavonoids in the treatment of gouty arthritis (Review).Molecular medicine reports · 2024Review
- The Inflammasome Adaptor Protein ASC in Plasma as a Biomarker of Early Cognitive Changes.International journal of molecular sciences · 2024Article
- Cerebral organoids with chromosome 21 trisomy secrete Alzheimer's disease-related soluble aggregates detectable by single-molecule-fluorescence and super-resolution microscopy.Molecular psychiatry · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Two key pathological hallmarks of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), are the accumulation of misfolded protein aggregates and the chronic progressive neuroinflammation that they trigger. Numerous original research and reviews have provided a comprehensive understanding of how aggregated proteins (amyloid β, pathological tau, and α-synuclein) contribute to the disease, including driving sterile inflammation, in part, through the aggregation of multi-protein inflammasome complexes and the ASC speck [composed of NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3), Apoptosis-associated speck-like protein containing a C-terminal caspase activation and recruitment domain (ASC), and inflammatory caspase-1] involved in innate immunity. Here, we provide a unique perspective on the crosstalk between the aggregation-prone proteins involved in AD/PD and the multi-protein inflammasome complex/ASC speck that fuels feed-forward exacerbation of each other, driving neurodegeneration. Failed turnover of protein aggregates (both AD/PD related aggregates and the ASC speck) by protein degradation pathways, prionoid propagation of inflammation by the ASC speck, cross-seeding of protein aggregation by the ASC speck, and pro-aggregatory cleavage of proteins by caspase-1 are some of the mechanisms that exacerbate disease progression. We also review studies that provide this causal framework and highlight how the ASC speck serves as a platform for the propagation and spreading of inflammation and protein aggregation that drives AD and PD.
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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.