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Spontaneous neurodegeneration in transgenic mice with mutant prion protein.

Transgenic mice were created to assess genetic linkage between Gerstmann-Sträussler-Scheinker syndrome and a leucine substitution at codon 102 of the human prion protein gene. Spontaneous neurologic disease with spongiform degeneration and gliosis similar to that in mouse scrapie developed at a mean age of 166 days in 35 mice expressing mouse prion protein with the leucine substitution. Thus, many of the clinical and pathological features of Gerstmann-Sträussler-Scheinker syndrome are reproduced in transgenic mice containing a prion protein with a single amino acid substitution, illustrating that a neurodegenerative process similar to a human disease can be genetically modeled in animals.[1]

References

  1. Spontaneous neurodegeneration in transgenic mice with mutant prion protein. Hsiao, K.K., Scott, M., Foster, D., Groth, D.F., DeArmond, S.J., Prusiner, S.B. Science (1990) [Pubmed]
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