NR AJBW
AU Ossa,J.E.; Machado,G.; Giraldo,M.A.; McEwen,J.G.
TI Prion plaques: molecular tumors. A hypothesis on the etiopathogenesis of prion diseases.
QU Medical Hypotheses 1995 Feb; 44(2): 124-6
PT journal article
AB In spite of remarkable advances in the etiopathogenesis of spongiform encephalopathies in man and animals and the growing acceptance of the prion hypothesis, there is no explanation for the supposed 'autocatalytic' activity of this protein molecule. Our molecular tumor hypothesis proposes that the prion protein is a genotoxin which interacts directly or indirectly but specifically with its homologous cellular gene introducing mutations which lead to aberrant processing and accumulation of the protein. It is also speculated that this hypothesis would shed some light on other diseases not presently classified as prion diseases and in the process of ageing.
IN Die Autoren mutmaßen, dass Prionproteine als Genotoxine Mutationen im Prionproteingen verursachen und damit die Produktion veränderter, akkumulierender Prionproteine bewirken könnten. Diese schwer nachvollziehbare Idee halten sie auch noch für die wahrscheinlichste Erklärung der bekannten Phänomene. Sie verstehen offensichtlich nicht viel von Proteinen.
ZR 24
MH Animal; Chromosomes, Human, Pair 20; *DNA Damage; DNA-Binding Proteins/genetics/*metabolism; Human; Mice; Mice, Transgenic; Models, Biological; Mutagenesis; Prion Diseases/*etiology/pathology; Prions/genetics/*metabolism
AD Facultad de Medicina, Universidad de Antioquia, Medellin, Colombia.
SP englisch
PO England
OR Prion-Krankheiten 6