ArticleJournal of virology2005
Comparison of inflammatory and acute-phase responses in the brain and peripheral organs of the ME7 model of prion disease.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- RETRACTED: Neuroinflammatory Markers: Key Indicators in the Pathology of Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2022Review
- High-Throughput Screening Platforms in the Discovery of Novel Drugs for Neurodegenerative Diseases.Bioengineering (Basel, Switzerland) · 2021Review
- Association of Osteoarthritis With Changes in Structural Neuroimaging Markers Over Time Among Non-demented Older Adults.Frontiers in aging neuroscience · 2021Article
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
- Review
- Article
- Defining the Microglia Response during the Time Course of Chronic Neurodegeneration.Journal of virology · 2015Article
- Interdependent and independent roles of type I interferons and IL-6 in innate immune, neuroinflammatory and sickness behaviour responses to systemic poly I:C.Brain, behavior, and immunity · 2015Article
- Prion infection of mouse brain reveals multiple new upregulated genes involved in neuroinflammation or signal transduction.Journal of virology · 2015Article
- Analysis of the hippocampal proteome in ME7 prion disease reveals a predominant astrocytic signature and highlights the brain-restricted production of clusterin in chronic neurodegeneration.The Journal of biological chemistry · 2014Article
- Article
- Prion disease and the innate immune system.Viruses · 2012Review
- Presence of an acute phase response in sheep with clinical classical scrapie.BMC veterinary research · 2012Article
- Inflammation and adaptive immunity in Parkinson's disease.Cold Spring Harbor perspectives in medicine · 2012Review
- Osteoarthritis accelerates and exacerbates Alzheimer's disease pathology in mice.Journal of neuroinflammation · 2011Article
- Exacerbation of CNS inflammation and neurodegeneration by systemic LPS treatment is independent of circulating IL-1β and IL-6.Journal of neuroinflammation · 2011Article
- β-Adrenergic receptor antagonism prevents anxiety-like behavior and microglial reactivity induced by repeated social defeat.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Parkinson's disease and systemic inflammation.Parkinson's disease · 2011Article
- Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's disease.Journal of neuroinflammation · 2011Article
- The role of microglia in synaptic stripping and synaptic degeneration: a revised perspective.ASN neuro · 2010Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Chronic neurodegenerative diseases such as prion disease and Alzheimer's disease (AD) are reported to be associated with microglial activation and increased brain and serum cytokines and acute-phase proteins (APPs). Unlike AD, prion disease is also associated with a peripheral component in that the presumed causative agent, PrPSc, also accumulates in the spleen and other lymphoreticular organs. It is unclear whether the reported systemic acute-phase response represents a systemic inflammatory response to prion disease or merely reflects central nervous system (CNS) inflammation. For this study, we investigated whether intracerebrally initiated prion disease (ME7 model) provokes splenic, hepatic, or brain inflammatory and acute-phase responses. We detected no significant elevation of proinflammatory cytokines or activation of macrophages in the spleens of these animals, despite clear PrPSc deposition. Similarly, at 19 weeks we detected no significant elevation of transcripts for the APPs serum amyloid A, complement C3, pentraxin 3, and alpha2-antiplasmin in the liver, despite CNS neurodegeneration and splenic PrPSc deposition at this time. However, despite the low CNS expression levels of proinflammatory cytokines, there was robust expression of these APPs in degenerating brains. These findings suggest that PrPSc is not a stimulus for splenic macrophages and that neither peripheral PrPSc deposition nor CNS neurodegeneration is sufficient to produce a systemic acute-phase response. We also propose that serum cytokine and APP measurements are not useful during preclinical disease. Possible consequences of the clear chronic elevation of APPs in the CNS are discussed.
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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.