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

HYPOTHESIS AND PREDICTIONS
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.


BACKGROUND
Aβ accumulation is characteristic of Alzheimer's disease (AD) but the accumulation does not correlate with cognitive decline, unlike the rates of glucose metabolism.


STRATEGY
We compared averaged and individual estimates of regional binding potentials of [11 C]Pittsburgh compound B to regionally averaged and individual values of metabolism of [18 F]fluorodeoxyglucose in brain regions of volunteers with AD.


SIGNIFICANCE
The claim explains the cognitive decline in some patients at a significantly lower level of Aβ deposition than in other patients, as well as the presence of cognitively healthy individuals with high Aβ accumulation. With further support of the hypothesis, the significance of Aβ accumulation in brains of patients with AD may require revision.