Temporary alteration of neuronal network communication is a protective response to redox imbalance that requires GPI-anchored prion protein

Cellular prion protein (PrP(C)) protects neurons against oxidative stress damage. This role is lost upon its misfolding into insoluble prions in prion diseases, and correlated with cytoskeletal breakdown and neurophysiological deficits. Here we used mouse neuronal models to assess how PrP(C) protect...

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Detalles Bibliográficos
Autores principales: Foliaki, Simote T., Wood, Aleksandar, Williams, Katie, Smith, Anna, Walters, Ryan O., Baune, Chase, Groveman, Bradley R., Haigh, Cathryn L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Research Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10196843/
https://www.ncbi.nlm.nih.gov/pubmed/37172395
http://dx.doi.org/10.1016/j.redox.2023.102733

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10196843/
https://www.ncbi.nlm.nih.gov/pubmed/37172395
http://dx.doi.org/10.1016/j.redox.2023.102733

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