ArticleFrontiers in cellular neuroscience2019
Discrimination of Prion Strain Targeting in the Central Nervous System via Reactive Astrocyte Heterogeneity in CD44 Expression.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Accurate genomic predictions for chronic wasting disease in North American elk.G3 (Bethesda, Md.) · 2026Article
- Single-Cell Dissection of the SPP1-CD44 Axis Reveals Microglia-Astrocyte Crosstalk Driving Neuroinflammation in Temporal Lobe Epilepsy.Molecular neurobiology · 2026Article
- Inflammatory microglia signals drive A1-like polarization of astrocytes even in the presence of HIV-1 Tat.Molecular neurobiology · 2025Article
- The Evolution of Experimental Rodent Models for Prion Diseases.Journal of neurochemistry · 2025Review
- A Systematic Review of Sporadic Creutzfeldt-Jakob Disease: Pathogenesis, Diagnosis, and Therapeutic Attempts.Neurology international · 2024Review
- 1-L Transcription in Prion Diseases.International journal of molecular sciences · 2024Article
- Cell adhesion molecule CD44 is dispensable for reactive astrocyte activation during prion disease.Scientific reports · 2024Article
- Interactions between Cytokines and the Pathogenesis of Prion Diseases: Insights and Implications.Brain sciences · 2024Review
- Review
- Strain-Dependent Morphology of Reactive Astrocytes in Human- and Animal-Vole-Adapted Prions.Biomolecules · 2023Article
- Prion strains: shining new light on old concepts.Cell and tissue research · 2023Review
- Microglia deficiency accelerates prion disease but does not enhance prion accumulation in the brain.Glia · 2022Article
- Astrocyte in prion disease: a double-edged sword.Neural regeneration research · 2022Review
- Single-cell sequencing of human midbrain reveals glial activation and a Parkinson-specific neuronal state.Brain : a journal of neurology · 2022Article
- Consequences of variability in α-synuclein fibril structure on strain biology.Acta neuropathologica · 2022Review
- Innate Immune Tolerance in Microglia Does Not Impact on Central Nervous System Prion Disease.Frontiers in cellular neuroscience · 2022Article
- Review
- The degree of astrocyte activation is predictive of the incubation time to prion disease.Acta neuropathologica communications · 2021Article
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Non-cell autonomous astrocyte-mediated neuronal toxicity in prion diseases.Acta neuropathologica communications · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases or transmissible spongiform encephalopathies are fatal, progressive, neurodegenerative, protein-misfolding disorders. Prion diseases may arise spontaneously, be inherited genetically or be acquired by infection and affect a variety of mammalian species including humans. Prion infections in the central nervous system (CNS) cause extensive neuropathology, including abnormal accumulations of misfolded host prion protein, vacuolar change resulting in sponge-like (spongiform) appearance of CNS tissue, neurodegeneration and reactive glial responses. Many different prion agent strains exist and these can differ based on disease duration, clinical signs and the targeting and distribution of the neuropathology in distinct brain areas. Reactive astrocytes are a prominent feature in the prion disease affected CNS as revealed by distinct morphological changes and upregulation of glial fibrillary acidic protein (GFAP). The CD44 antigen is a transmembrane glycoprotein involved in cell-cell interactions, cell adhesion and migration. Here we show that CD44 is also highly expressed in a subset of reactive astrocytes in regions of the CNS targeted by prions. Astrocyte heterogeneity revealed by differential CD44 upregulation occurs coincident with the earliest neuropathological changes during the pre-clinical phase of disease, and is not affected by the route of infection. The expression and distribution of CD44 was compared in brains from a large collection of 15 distinct prion agent strains transmitted to mice of different prion protein (
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