Experimental study reveals fibrinogen binding to cellular prion protein activates neurotoxic pathways in mouse astrocytes, suggesting a mechanism for astrocyte-driven neurodegeneration.
For the first time we showed that fibrinogen (Fg) can associate with cellular prion protein (PrP C ) on the surface of cultured mouse brain astrocytes. At high levels, Fg causes upregulation of astrocyte PrP C and astrocyte activation accompanied with overexpression of tyrosine receptor kinase B (TrkB), which results in nitric oxide (NO) production and generation of reactive oxygen species (ROS). Fg/PrP C interaction can be a triggering mechanism for TrkB-NO-ROS axis activation and the resultant astrocyte-mediated neurodegeneration.
No takes yet. Share an insight, caveat, or question.
Charkviani et al. (2020) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: