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Therapies for human prion diseases.

Peter K Panegyres¹, Elizabeth Armari

¹Neurodegenerative Disorders Research Pty Ltd 185 York St, Subiaco WA, Australia.

American Journal of Neurodegenerative Disease

|October 5, 2013

Summary

Human prion diseases stem from misfolded prion proteins (PrP). Therapeutic strategies targeting PrP conversion and related pathways show promise for treating these devastating neurodegenerative disorders.

Keywords:

Creutzfeldt-Jakob disease Prion diseases neurodegenerative diseases protein misfolding protein propagation treatments

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Area of Science:

Neuroscience
Biochemistry
Pathology

Background:

Human prion diseases involve the conversion of normal prion protein (PrP(c)) to a pathological form (PrP(res)).
This conversion leads to neurodegeneration and amyloid plaque formation.
Protein misfolding is a common mechanism in various neurodegenerative diseases.

Purpose of the Study:

To explore the pathological mechanisms of human prion diseases.
To review potential therapeutic strategies for prion diseases.
To highlight the broader implications of anti-prion agents for other neurodegenerative disorders.

Main Methods:

Review of existing literature on prion protein conversion and therapeutic interventions.
Analysis of drug mechanisms, including polyanionic compounds like pentosan polysulfate (PPS).
Examination of emerging therapeutic approaches targeting the laminin receptor.

Main Results:

Pentosan polysulfate (PPS) and similar compounds may inhibit PrP(c) to PrP(res) conversion and help clear PrP(res).
Therapeutic strategies targeting the laminin receptor show experimental promise.
The shared protein misfolding mechanism suggests potential cross-application of treatments.

Conclusions:

Effective anti-prion agents could have significant implications for a range of neurodegenerative diseases.
Targeting PrP conversion and associated pathways offers a viable therapeutic avenue.
Further research into neuroprotection, immunotherapy, and nucleic acid-based therapies is warranted.