Detecting Aβ *56 oligomers in brain tissues

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)peer-review

31 Scopus citations


Since its original description in 1906 by Dr Alois Alzheimer, amyloid plaques and neurofibrillary tangles have remained the hypothetical cause of Alzheimer's disease. However, plaque burden poorly predicts cognitive status in humans, which led several groups to investigate the possibility that soluble species of amyloid-beta (Aβ) peptides could be playing an important pathological function in the aging brain. Through a multistep fractionation protocol, we identified a 56 kDa oligomer of Aβ, termed Aβ, 56, the amount of which correlates with cognitive impairment. Here, we describe our biochemical approach to isolate this oligomeric Aβ species in brain tissue of transgenic mouse models of AD.

Original languageEnglish (US)
Title of host publicationAlzheimers Disease and Frontotemporal Dementia
Subtitle of host publicationMethods and Protocols
PublisherHumana Press Inc.
Number of pages12
ISBN (Print)9781607617433
StatePublished - May 11 2011

Publication series

NameMethods in molecular biology (Clifton, N.J.)
PublisherHumana Press
ISSN (Print)1064-3745


  • Alzheimer
  • Amyloid-beta (Aβ)
  • Brain
  • Transgenic mouse model
  • Western blotting


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