Abstract
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.
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© 2010 Humana Press
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Sherman, M.A., Lesné, S.E. (2010). Detecting Aβ*56 Oligomers in Brain Tissues. In: Roberson, E. (eds) Alzheimer's Disease and Frontotemporal Dementia. Methods in Molecular Biology, vol 670. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60761-744-0_4
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DOI: https://doi.org/10.1007/978-1-60761-744-0_4
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