PET amyloid imaging does a fine job finding susceptibility to Alzheimer’s disease long before symptoms set in, but PET tau imaging is better at showing what’s going on once neuronal injury becomes functionally evident.
That’s the conclusion of Alexander Drzezga, MD, of the University Hospital of Cologne in Germany, who presented his research team’s findings June 13 at the annual meeting of the Society of Nuclear Medicine and Molecular Imaging (SNMMI) in San Diego.
Drzezga and colleagues analyzed the cases of 10 Alzheimer’s patients who underwent PET augmented by three radiotracers—fluorine-18 fluorodeoxyglucose (F-18 FDG), which images regional metabolic activity; carbon-11 Pittsburgh compound B (C-11 PiB), which has an affinity for amyloid plaques; and F-18 AV-1451, an emerging imaging agent that binds to tau in the brain.
According to news reported by SNMMI from the conference, results showed that increased neurofibrillary tangles of tau proteins were directly associated with hypometabolism (reflecting neuronal dysfunction) in the brain.
For amyloid deposition, no strong association with hypometabolism was found. However, the team observed an indirect interactivity between tau and amyloid, particularly in the parietal cortex: The negative impact of regional tau deposition on metabolism was stronger in regions with higher amyloid-burden.
“Integrating these molecular imaging tools offers the opportunity to investigate the possible independent and synergistic contribution of these protein pathologies in neurodegeneration in the living brain and, therefore, greatly advances our understanding of the mechanisms of Alzheimer’s disease,” Drzezga said.
SNMMI adds in its news item that multimodal imaging approaches like the one demonstrated by Drzezga and team “could allow more precise staging of neuropathology, even before the irrevocable onset of memory loss experienced by Alzheimer’s patients.”