ArticleScientific reports2016
Astrocyte-to-neuron intercellular prion transfer is mediated by cell-cell contact.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 88 citations in OpenAlex.
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- Stereotaxic Delivery of M1000 Prions to the Hippocampus Induces Related Behavioural and Cognitive Changes Consistent with Acute Neurotoxic Effects.Molecular neurobiology · 2025Article
- Glial phagocytosis for synapse and toxic proteins in neurodegenerative diseases.Molecular neurodegeneration · 2025Review
- Microglia-specific NF-κB signaling is a critical regulator of prion-induced glial inflammation and neuronal loss.PLoS pathogens · 2025Article
- Lipid metabolism, remodelling and intercellular transfer in the CNS.Nature reviews. Neuroscience · 2025Review
- Dysregulation of protein degradation and alteration of secretome in α-synuclein-exposed astrocytes: implications for dopaminergic neuronal dysfunction.Cell communication and signaling : CCS · 2024Article
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- Intercellular Highways in Transport Processes.Results and problems in cell differentiation · 2024Review
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- Strain-Dependent Morphology of Reactive Astrocytes in Human- and Animal-Vole-Adapted Prions.Biomolecules · 2023Article
- Genetically engineered cellular models of prion propagation.Cell and tissue research · 2023Review
- Hijacking intercellular trafficking for the spread of protein aggregates in neurodegenerative diseases: a focus on tunneling nanotubes (TNTs).Extracellular vesicles and circulating nucleic acids · 2023Review
- Adipose-derived mesenchymal stromal cells decrease prion-induced glial inflammation in vitro.Scientific reports · 2022Article
- Glial activation in prion diseases is selectively triggered by neuronal PrPBrain pathology (Zurich, Switzerland) · 2022Article
- Present and future avenues of cell-based therapy for brain injury: The enteric nervous system as a potential cell source.Brain pathology (Zurich, Switzerland) · 2022Review
- Astrocyte in prion disease: a double-edged sword.Neural regeneration research · 2022Review
- The role of astrocytes in prion-like mechanisms of neurodegeneration.Brain : a journal of neurology · 2022Review
- Propagation and Dissemination Strategies of Transmissible Spongiform Encephalopathy Agents in Mammalian Cells.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases are caused by misfolding of the cellular protein PrP(C) to an infectious conformer, PrP(Sc). Intercellular PrP(Sc) transfer propagates conversion and allows infectivity to move from the periphery to the brain. However, how prions spread between cells of the central nervous system is unclear. Astrocytes are specialized non-neuronal cells within the brain that have a number of functions indispensable for brain homeostasis. Interestingly, they are one of the earliest sites of prion accumulation in the brain. A fundamental question arising from this observation is whether these cells are involved in intercellular prion transfer and thereby disease propagation. Using co-culture systems between primary infected astrocytes and granule neurons or neuronal cell lines, we provide direct evidence that prion-infected astrocytes can disseminate prion to neurons. Though astrocytes are capable of secreting PrP, this is an inefficient method of transferring prion infectivity. Efficient transfer required co-culturing and direct cell contact. Astrocytes form numerous intercellular connections including tunneling nanotubes, containing PrP(Sc), often colocalized with endolysosomal vesicles, which may constitute the major mechanism of transfer. Because of their role in intercellular transfer of prions astrocytes may influence progression of the disease.
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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.