PrP and beta-amyloid fragments activate different neurotoxic mechanisms in cultured mouse cells.

@article{Brown1997PrPAB,
  title={PrP and beta-amyloid fragments activate different neurotoxic mechanisms in cultured mouse cells.},
  author={David R Brown and Jochen Herms and Bernhard M. W. Schmidt and Hans A. Kretzschmar},
  journal={The European journal of neuroscience},
  year={1997},
  volume={9 6},
  pages={1162-9}
}
Alzheimer's disease and prion diseases such as Creutzfeldt-Jakob disease are caused by as yet undefined metabolic disturbances of normal cellular proteins, the amyloid precursor protein and the prion protein (PrP). Synthetic fragments of both proteins, beta-amyloid 25-35 (betaA25-35) and PrP106-126, have been shown to be toxic to neurons in culture. Cell death in both cases occurs by apoptosis. Here we show that there are considerable differences in the mechanisms involved. Thus, PrP106-126 is… CONTINUE READING

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