ArticleFrontiers in aging neuroscience2014
Subtype and regional-specific neuroinflammation in sporadic creutzfeldt-jakob disease.
Article in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 67 citations in OpenAlex.
- Cross-Omic Comparative Analysis Identifies Transcriptomic Signatures and Exploratory Gene Set-Level Signals in Sporadic Creutzfeldt-Jakob Disease.International journal of molecular sciences · 2026Article
- Preclinical serum alterations and tissue changes in protein and gene expression of early cerebrospinal fluid-validated biomarkers in scrapie.Veterinary research · 2026Article
- New preclinical biomarkers for prion diseases in the cerebrospinal fluid proteome revealed by mass spectrometry.The veterinary quarterly · 2024Article
- The Neuroimmune System and the Cerebellum.Cerebellum (London, England) · 2024Review
- Rapid progression of probable Creutzfeldt-Jakob disease with concomitant COVID-19 infection.BMJ case reports · 2023Article
- Genetic analysis of potential biomarkers and therapeutic targets in neuroinflammation from sporadic Creutzfeldt-Jakob disease.Scientific reports · 2023Article
- Molecular Mechanisms Underlying Neuroinflammation Elicited by Occupational Injuries and Toxicants.International journal of molecular sciences · 2023Review
- Enhanced M-CSF/CSF1R Signaling Closely Associates with PrPMolecular neurobiology · 2022Article
- Review
- Distinctive Toll-like Receptors Gene Expression and Glial Response in Different Brain Regions of Natural Scrapie.International journal of molecular sciences · 2022Article
- The roles of Eph receptors, neuropilin-1, P2X7, and CD147 in COVID-19-associated neurodegenerative diseases: inflammasome and JaK inhibitors as potential promising therapies.Cellular & molecular biology letters · 2022Review
- Differential astrocyte and oligodendrocyte vulnerability in murine Creutzfeldt-Jakob disease.Prion · 2021Article
- Article
- The role of microglia in prion diseases and possible therapeutic targets: a literature review.Prion · 2021Review
- TREM2 expression in the brain and biological fluids in prion diseases.Acta neuropathologica · 2021Article
- Neuroimmune Response Mediated by Cytokines in Natural Scrapie after Chronic Dexamethasone Treatment.Biomolecules · 2021Article
- Regional Differences in Neuroinflammation-Associated Gene Expression in the Brain of Sporadic Creutzfeldt-Jakob Disease Patients.International journal of molecular sciences · 2020Article
- Administration of FK506 from Late Stage of Disease Prolongs Survival of Human Prion-Inoculated Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Article
- Neuroimmune Response in Natural Preclinical Scrapie after Dexamethasone Treatment.International journal of molecular sciences · 2020Article
- Assessment of Glial Activation Response in the Progress of Natural Scrapie after Chronic Dexamethasone Treatment.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study identifies deregulated cytokines and mediators of the immune response in the frontal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease (sCJD) MM1 and VV2 subtypes compared to age-matched controls. Deregulated genes include pro- and anti-inflammatory cytokines, toll-like receptors, colony stimulating factors, cathepsins, members of the complement system, and members of the integrin and CTL/CTLD family with particular regional and sCJD subtype patterns. Analysis of cytokines and mediators at protein level shows expression of selected molecules and receptors in neurons, in astrocytes, and/or in microglia, thus suggesting interactions between neurons and glial cells, mainly microglia, in the neuroinflammatory response in sCJD. Similar inflammatory responses have been shown in the tg340 sCJD MM1 mice, revealing a progressive deregulation of inflammatory mediators with disease progression. Yet, inflammatory molecules involved are subjected to species differences in humans and mice. Moreover, inflammatory-related cell signaling pathways NFκB/IKK and JAK/STAT are activated in sCJD and sCJD MM1 mice. Together, the present observations show a self-sustained complex inflammatory and inflammatory-related responses occurring already at early clinical stages in animal model and dramatically progressing at advanced stages of sCJD. Considering this scenario, measures tailored to modulate (activate or inhibit) specific molecules could be therapeutic options in CJD.
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