ArticlePloS one2017
Cystatin F is a biomarker of prion pathogenesis in mice.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- APOE genotype differentially modulates prion pathology in a mouse model.Acta neuropathologica communications · 2026Article
- APOE Genotype Differentially Modulates Prion Pathology in a Mouse Model.Research square · 2025Article
- Cystatin F-a key player in central nervous system disease.Journal of neuroinflammation · 2025Review
- Microglia contribute to polyG-dependent neurodegeneration in neuronal intranuclear inclusion disease.Acta neuropathologica · 2024Article
- Single-Cell RNA-seq reveals transcriptomic modulation of Alzheimer's disease by activated protein C.Aging · 2024Article
- Cystatin F (eLife · 2023Article
- Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Cystatin F acts as a mediator of immune suppression in glioblastoma.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- NEK1-mediated retromer trafficking promotes blood-brain barrier integrity by regulating glucose metabolism and RIPK1 activation.Nature communications · 2021Article
- Core transcriptional regulatory circuits in prion diseases.Molecular brain · 2020Article
- Targeting RIPK1 for the treatment of human diseases.Proceedings of the National Academy of Sciences of the United States of America · 2019Review
- Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases.Nature reviews. Neuroscience · 2019Review
- Prion pathogenesis is unaltered in a mouse strain with a permeable blood-brain barrier.PLoS pathogens · 2018Article
- Lymphocyte activation gene 3 (Lag3) expression is increased in prion infections but does not modify disease progression.Scientific reports · 2018Article
- RIPK1 mediates a disease-associated microglial response in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- RIPK1 promotes inflammation and β-amyloid accumulation in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Prion pathogenesis is unaltered in the absence of SIRPα-mediated "don't-eat-me" signaling.PloS one · 2017Article
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Misfolding of the cellular prion protein (PrPC) into the scrapie prion protein (PrPSc) results in progressive, fatal, transmissible neurodegenerative conditions termed prion diseases. Experimental and epidemiological evidence point toward a protracted, clinically silent phase in prion diseases, yet there is no diagnostic test capable of identifying asymptomatic individuals incubating prions. In an effort to identify early biomarkers of prion diseases, we have compared global transcriptional profiles in brains from pre-symptomatic prion-infected mice and controls. We identified Cst7, which encodes cystatin F, as the most strongly upregulated transcript in this model. Early and robust upregulation of Cst7 mRNA levels and of its cognate protein was validated in additional mouse models of prion disease. Surprisingly, we found no significant increase in cystatin F levels in both cerebrospinal fluid or brain parenchyma of patients with Creutzfeldt-Jakob disease compared to Alzheimer's disease or non-demented controls. Our results validate cystatin F as a useful biomarker of early pathogenesis in experimental models of prion disease, and point to unexpected species-specific differences in the transcriptional responses to prion infections.
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