Amyloid burden and neural function in people at risk for AD


Johnson SC, Christian BT, Okonkwo OC, Oh J, Harding S, Xu G, Hillmer AT, Wooten DW, Murali D, Barnhart T, Hall LT, Racine AM, Klunk WE, Mathis CA, Bendlin BB, Gallagher CL, Carlsson CM, Rowley HA, Hermann BP, Dowling NM, Asthana S, Sager MA

Neurobiol Aging. 2014 Mar;35(3):576-84.

Abstract

To determine the relationship between amyloid burden and neural function in healthy adults at risk for Alzheimer’s Disease (AD), we used multi-modal imaging with [C-11]Pittsburgh Compound B positron emission tomography (PET), [F-18]Fluorodeoxyglucose (FDG) PET and MRI, together with cognitive measurement in 201 subjects (mean age 60.1, range 46 to 73) from the Wisconsin Registry for Alzheimer’s Prevention (WRAP). Using a qualitative rating, 18% of the sample were strongly amyloid positive (Aβ+), 41% indeterminate (Aβi) and 41% negative (Aβ-). Aβ+ was associated with older age, female sex, and showed trends for maternal family history of AD and APOE4. Relative to the Aβ- group, Aβ+ and Aβi participants had increased glucose metabolism in the bilateral thalamus; Aβ+ participants also had increased metabolism in the bilateral superior temporal gyrus. Aβ+ participants exhibited increased GM in the lateral parietal lobe bilaterally relative to the Aβ- group, and no areas of significant atrophy. Cognitive performance and self report cognitive and affective symptoms did not differ between groups. Amyloid burden can be identified in adults at a mean age of 60 and is accompanied by glucometabolic increases in specific areas, but not atrophy or cognitive loss. This asymptomatic stage may be an opportune window for intervention to prevent progression to symptomatic AD.

PDF

Contributing Lab Members