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Related Experiment Video

Updated: Feb 2, 2026

Detection of Abnormal Prion Protein by Immunohistochemistry

Detection of Abnormal Prion Protein by Immunohistochemistry

Published on: May 5, 2023

The prion protein in neuroimmune crosstalk.

Øyvind Salvesen¹, Jörg Tatzelt², Michael A Tranulis³

¹Faculty of Veterinary Medicine, Department of Production Animal Clinical Sciences, Norwegian University of Life Sciences, Sandnes, Norway.

Neurochemistry International

|November 19, 2018

Summary

The cellular prion protein (PrP^C) is crucial for prion disease development and neurotoxicity. Understanding its role in immune signaling is key for developing treatments targeting these harmful conditions.

Keywords:

Cellular prion protein Immune signaling Inflammation Neuroimmune crosstalk Proteolytic cleavage

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Area of Science:

Neuroscience
Immunology
Molecular Biology

Background:

The cellular prion protein (PrP^C) is a cell surface glycoprotein encoded by the PRNP gene.
PrP^C is abundant in the central nervous system and present in immune cells.
While not essential for life, PrP^C plays a critical role in prion diseases.

Purpose of the Study:

To summarize research on the role of PrP^C in cellular processes.
To highlight PrP^C's involvement in immune signaling and neuroimmune crosstalk.
To emphasize PrP^C as a potential therapeutic target for prion diseases.

Main Methods:

Review of experimental knockout studies in various animal models.
Analysis of data from naturally occurring mutations affecting PrP^C synthesis.
Synthesis of recent research findings on PrP^C function.

Main Results:

Loss of PrP^C does not cause discernible phenotypes but prevents prion disease.
PrP^C converts to a pathogenic form (PrP^Sc) causing neurodegeneration.
Endogenous PrP^C acts as a toxic receptor in prion-induced neurotoxicity.

Conclusions:

PrP^C is central to prion pathogenesis and neurotoxicity.
Understanding PrP^C's role in immune modulation is vital for therapeutic strategies.
Further research into PrP^C's physiological functions is warranted.