Kuru: Its ramifications after fifty years

@article{Liberski2009KuruIR,
  title={Kuru: Its ramifications after fifty years},
  author={Pawel P. Liberski and Paul W. Brown},
  journal={Experimental Gerontology},
  year={2009},
  volume={44},
  pages={63-69}
}
Kuru was the first human neurodegenerative disease in the group of transmissible spongiform encephalopathies, prion diseases or, in the past, slow unconventional virus diseases. It was reported to Western medicine in 1957 by Gajdusek and Zigas. Kuru was spread by endocannibalism and because of this the ratio of affected women and children to men was excessive. The hallmark of kuru neuropathology is the amyloid plaque. We may speculate what would happen if kuru had not been discovered or did not… 
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TLDR
The discovery of kuru opened new vistas of human medicine and was pivotal in the subsequent transmission of Creutzfeldt–Jakob disease, as well as the relevance that bovine spongiform encephalopathy had for transmission to humans.
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TLDR
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TLDR
Concerns are raised that various protein misfolding diseases might have spreading, prion-like etiologies that contribute to pathogenesis or prevalence.
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TLDR
The discovery of kuru opened new windows into the realms of human medicine and was instrumental in the later transmission of Creutzfeldt-Jakob disease and Gerstmann-Sträussler-Scheinker disease as well as the relevance that bovine spongiform encephalopathy had for transmission to humans.
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TLDR
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A Quick Method to Evaluate the Effect of the Amino Acid Sequence in the Misfolding Proneness of the Prion Protein.
TLDR
A new method in vitro to assess and quantify the PrP misfolding phenomenon in order to better understand the molecular mechanisms involved in this process.
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