We hypothesize that Alzheimer's disease (AD) has a preclinical stage in which elevated levels of brainamyloid protein and accumulation of beta-amyloid deposits foreshadow the gradual onset of neuronaldysfunction, cell loss and dementia. While the exact role of amyloid in the initiation of brain damage is stillunclear, clarifying the exact timing of amyloid deposition that precede AD would be extremely helpful inunderstanding the biological origins of AD and in designing appropriate interventions. Brain imaging providesa window into many of the hypothesized biochemical, functional and anatomic changes in AD. With PositronEmission Tomography (PET) using [11C]PIB it is possible to estimate the density of beta-amyloid plaques byimaging the PIB binding sites. With PET using [18F]FDG it is possible to estimate neuronal function frommeasures of metabolic activity. Finally, with magnetic resonance imaging (MRI) volume loss over time canbe quantified in regional and global brain measures. It is our premise that by examining the temporal andspatial interrelationships between these three measures important insights will be gained in thepathophysiology of AD.The value of these imaging biomarkers are further enhanced by combining the data with CSF biomarkersand clinical and psychometric data. Towards these goals, the Imaging Core will provide two key supportactivities to the DIAN effort:
Aim 1 : Oversee the collection of all image data. This data includes MR scansfor morphometrics, PET FDG scans for metabolism and PET PIB scans for imaging beta-amyloid plaques.
Aim 2 : Perform image processing and analysis to extract biologically relevant measures from the image dataset. These measures include whole brain volume and cortical and subcortical regional measures of graymatter volume, relative glucose metabolism and PIB-derived estimates of beta-amyloid plaque deposition.
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