Amyloid plaque burden has been linked with hypometabolism of neurons in areas of the brain associated with Alzheimer’s disease, according to the results of a study presented at the Society of Nuclear Medicine and Molecular Imaging’s 2013 annual meeting in Vancouver.

The association between lower metabolism and amyloid plaque was shown in people with no sign of cognitive decline, meaning the results could represent a potential Alzheimer’s precursor, according to Val J. Lowe, MD, of the Mayo Clinic Cancer Center in Rochester, Minn., and colleagues.

“Previous studies indicate that hypometabolism of this same pattern is present in patients who have abnormalities of the gene apolipoprotein E, or APOE,” Lowe said in a release. “The hypothesis is that people who have these genetic abnormalities tend to have hypometabolism and are on the trajectory toward developing Alzheimer’s disease. Hypometabolism does appear to be an early harbinger of the disease before dementia sets in.”

The research is part of the Mayo Clinic Study of Aging, a longitudinal, multi-phase study currently including 2,500 patients. A total of 617 cognitively normal subjects were included in this imaging study, and all underwent two PET scans—the first with C-11 Pittsburgh compound B (PiB) to identify amyloid burden, and the second, an hour later, with F-18 FDG to show metabolism.

Lowe and colleagues found significant hypometabolism in the angular gyrus and posterior cingulate, regions associated with Alzheimer’s disease, even when PiB PET scans were barely positive for amyloid.

The conclusions were based on group-wide findings, and in an email to Health Imaging, Lowe wrote, “We will need to wait to see if we can identify the same changes in individual patients.”