Prions, prionoids and pathogenic proteins in Alzheimer disease

Karen H. Ashe, Adriano Aguzzi

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

Like patients with prion disease, Alzheimer patients suffer from a fatal, progressive form of dementia. There is growing evidence that amyloid-β (Aβ) aggregates may be transmissible similar to prions, at least under extreme experimental conditions. However, unlike mice infected with prion protein (PrP) prions, those inoculated with Aβ do not die. The transmission of Aβ and PrP thus differs conspicuously in the neurological effects they induce in their hosts, the difference being no less than a matter of life and death. Far from being a mere academic nuance, this distinction between Aβ and PrP begs the crucial questions of what, exactly, controls prion toxicity and how prion toxicity relates to prion infectivity.

Original languageEnglish (US)
Pages (from-to)55-59
Number of pages5
JournalPrion
Volume7
Issue number1
DOIs
StatePublished - Jan 1 2013

Fingerprint

Prions
Alzheimer Disease
Proteins
Toxicity
Prion Diseases
Amyloid
Dementia
Prion Proteins

Keywords

  • Alzheimer disease
  • Amyloid-β
  • Pathogenic proteins
  • PrP
  • Prionoids
  • Prions
  • Tau

Cite this

Prions, prionoids and pathogenic proteins in Alzheimer disease. / Ashe, Karen H.; Aguzzi, Adriano.

In: Prion, Vol. 7, No. 1, 01.01.2013, p. 55-59.

Research output: Contribution to journalArticle

Ashe, Karen H. ; Aguzzi, Adriano. / Prions, prionoids and pathogenic proteins in Alzheimer disease. In: Prion. 2013 ; Vol. 7, No. 1. pp. 55-59.
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