This article compares the amyloid cascade hypothesis and the mitochondrial cascade hypothesis for sporadic Alzheimer's disease and discusses biomarkers for its preclinical phase. It states that ketone ester-induced elevation of plasma ketone body levels improves mitochondrial metabolism and prevents or delays progression of AD-like pathologic changes in several AD animal models. The authors conclude that, as a first step, it is imperative to determine whether ketone ester-caused hyperketonemia can bring about favorable changes in biomarkers of AD pathology in people in an early stage of preclinical AD.
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