I recommend this paper
This paper corroborates neuropathological findings: amyloid deposition can be found in non-demented patients. Correlation with cognitive deficits comes with intensification of amyloidosis and, most importantly, the extension of tau pathology.
Question: why are Abeta oligomers, protofibrils and amyloid deposits observed in non-demented patients not toxic?
Several hypotheses: neuronal reservoir, compensation, not-detectable MCI, or simply that they are not toxic in the human brain, but toxic in the experimental models constructed to demonstrate a toxicity.
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