Fig. 3

Alternative versions of the plaque buffering of soluble Aβ aggregate hypothesis. The overall hypothesis states that plaques may buffer soluble Aβ aggregates, protecting neuronal structures from toxicity at early times and then releasing toxic aggregates at later times. a Sub-hypothesis that qualitative changes in the soluble aggregates correlate with dementia: The soluble aggregates from non-demented controls could be readily buffered by plaques, but the soluble aggregates from demented patients would not be well buffered by plaques. b Sub-hypothesis that qualitative changes in the plaques correlate with dementia: The plaques from non-demented controls would retain more buffering capacity than the plaques from demented patients. c Sub-hypothesis that quantitative changes in the soluble Aβ aggregates correlate with dementia: The intrinsic buffering properties of soluble Aβ aggregates and plaques from non-demented controls would be similar to those of demented patients when assessed using the same concentrations of soluble Aβ aggregates. (Original figure: D. Brody)