In Alzheimer's disease, amyloid beta accumulation is a protective mechanism that ultimately fails.

Abstract

Here, we claim that amyloid beta (Aβ) accumulation is a protective mechanism that ultimately fails. We predict that more Aβ accumulates in regions with higher rates of glucose metabolism, reaching a maximum followed by progression of pathology. Aβ accumulation is characteristic of Alzheimer's disease (AD) but the accumulation does not correlate with cognitive decline, unlike the rates of glucose metabolism. We compared averaged and individual estimates of regional binding potentials of [11C]Pittsburgh compound B to regionally averaged and individual values of metabolism of [18F]fluorodeoxyglucose in brain regions of volunteers with AD. The claim explains the cognitive decline in some patients at a significantly lower level of Aβdeposition than in other patients, as well as the presence of cognitively healthy individuals with high Aβaccumulation. With further support of the hypothesis, the significance of Aβaccumulation in brains of patients with AD may require revision.