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Targeting Prion Protein and Alzheimer's disease Amyloid Peptide by Peptide Ligands

D Willbold, K Wiesehan, K Haenel, S Patt, RP Linke · Klinische Neurophysiologie · 2004 · Heft 08

Dokument
909173
CareLit-ID
Jahr
2004
Publikation
PDF
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Metadaten
DOI
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Bibliografische Angaben

Zeitschrift
Klinische Neurophysiologie
Autor:innen
D Willbold, K Wiesehan, K Haenel, S Patt, RP Linke
Ausgabe
Heft 08 / 2004
Seiten
–
Erschienen: 2004-08-25 00:00:00
ISSN
1434-0275

Zusammenfassung

The presently established models of prion propagation are based on the essential role of the host-encoded prion protein (PrP). Development and progression of the disease implies ongoing conversion of its non-pathological isoform PrPC into its pathological isoform PrPSc. Thus, any stabilization of the PrPC conformation should slow down or inhibit conversion of PrPC into PrPSc. We screened a phage displayed peptide library to ultimately identify high affinity ligands that bind to and stabilize PrPC. A similar approach was used to identify ligands that specifically bind to Alzheimer's disease (AD) amyloid peptide A…

Schlagworte

Klinische Neurophysiologie