Posterior Cingulate Glucose Metabolism, Hippocampal Glucose Metabolism, and Hippocampal Volume in Cognitively Normal, Late-Middle-Aged Persons at 3 Levels of Genetic Risk for Alzheimer Disease

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Abstract
We and others have been using positron emission tomography (PET) measurements of the cerebral metabolic rate for glucose (CMRgl) in the posterior cingulate cortex and other brain regions that are known to be preferentially affected by Alzheimer disease (AD), magnetic resonance imaging (MRI) measurements of hippocampal and other brain tissue volumes, and other biomarker measurements to detect and track some of the brain changes that precede the clinical onset of AD.1-12 These findings have led our group and others to consider how these biomarkers could be used for people at increased risk for AD in the accelerated evaluation of presymptomatic AD treatments.8,12-14 They have also led researchers to propose models that characterize the trajectory of different biomarker changes associated with the preclinical stages of the disorder.15,16 For instance, 18F-fluorodeoxyglucose (FDG)–PET studies17-24 reveal characteristic and progressive CMRgl reductions in the posterior cingulate, precuneus, and parietal, temporal, and prefrontal brain regions beginning years before the clinical onset of AD. In other studies, we have reported evidence of CMRgl reductions in an automatically characterized hippocampal region of interest; these reductions were associated with apparent normal aging and predicted future cognitive decline.5 Magnetic resonance imaging studies reveal progressively reduced hippocampal volumes, which tend to parallel the earliest memory changes that herald the clinical onset of AD.25

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