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Human prion strain selection in transgenic mice.

Kurt Giles1, David V Glidden, Smita Patel

  • 1Institute for Neurodegenerative Diseases, University of California at San Francisco, 94143-0518, USA.

Annals of Neurology
|August 10, 2010
PubMed
Summary
This summary is machine-generated.

Two transgenic mouse lines expressing chimeric prion proteins offer rapid models for studying human prion diseases. These models show accelerated incubation periods for Creutzfeldt-Jakob disease (CJD) strains, aiding research into prion disease evolution.

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Area of Science:

  • Neuroscience
  • Genetics
  • Pathology

Background:

  • Transgenic (Tg) mice expressing chimeric mouse/human prion proteins (PrPs) exhibit shorter incubation periods for Creutzfeldt-Jakob disease (CJD) prions compared to mice with full-length human PrP.
  • Modifying chimeric PrP sequence similarity to mouse PrP enhances susceptibility to CJD prions.

Purpose of the Study:

  • To develop and characterize novel transgenic mouse models for studying human prion diseases.
  • To investigate the impact of specific amino acid changes in chimeric PrP on prion disease incubation periods and strain evolution.

Main Methods:

  • Generation of transgenic mouse lines expressing chimeric mouse/human PrP.
  • Intracerebral inoculation of mice with Creutzfeldt-Jakob disease (CJD) prion strains (sporadic and variant).
  • Monitoring neurological dysfunction for incubation time determination and post-mortem analysis of PrP(Sc) and neuropathology.

Main Results:

  • A Tg mouse line (Tg22372) showed susceptibility to sporadic CJD (sCJD) prions in approximately 110 days.
  • A further modified Tg line (Tg1014) exhibited susceptibility to sCJD prions in approximately 75 days.
  • Tg1014 mice demonstrated shorter incubation periods for variant CJD (vCJD) prions and facilitated the study of vCJD prion strain evolution, yielding both vCJD-like and sCJD-like strains.

Conclusions:

  • The developed Tg mouse lines (Tg22372 and Tg1014) serve as valuable, rapid models for studying human prion diseases.
  • These models enable the investigation of prion strain evolution and the selective pressure influencing prion propagation.