Cerebral Amyloid Angiopathy Pathology and Its Association With Amyloid-β PET Signal
Stuart J. McCarter, Timothy G. Lesnick, Val J. Lowe, Michelle M. Mielke, Eleni Constantopoulos, Alejandro A. Rabinstein, Scott A. Przybelski, Hugo Botha, David T. Jones, Vijay K. Ramanan, Clifford R. Jack, Ronald C. Petersen, David S. Knopman, Bradley F. Boeve, Melissa E. Murray, Dennis W. Dickson, Prashanthi Vemuri, Kejal Kantarci, R. Ross Reichard, Jonathan Graff‐Radford
Abstract
BACKGROUND AND OBJECTIVES: To determine the contribution of cerebral amyloid angiopathy (CAA) to Pittsburgh compound B (PiB)-PET tracer retention. METHODS: Participants from the Mayo Clinic Study of Aging and Mayo Clinic Alzheimer's Disease Research Center with antemortem PiB-PET imaging for β-amyloid (Aβ) who later underwent autopsy were included in this study. Pathologic regional leptomeningeal, parenchymal, capillary CAA, and Aβ plaque burden were calculated from one hemisphere. Regional lobar amyloid standardized uptake value ratio (SUVR) on PET was calculated from the same hemisphere sampled at autopsy. Single- and multiple-predictor linear regression models were used to evaluate the relative contributions of pathologically determined regional CAA and Aβ plaques to antemortem PiB-PET SUVR. RESULTS: < 0.05). In patients without frequent amyloid plaques, CAA was not associated with PiB-PET in any region. DISCUSSION: We did not find evidence that pathologically confirmed regional CAA burden contributes significantly to proximal antemortem regional PiB-PET signal, suggesting that amyloid PET imaging for measurement of cortical amyloid burden is unconfounded by CAA on a lobar level. Whether CAA burden contributes to PiB-PET signal in patients with severe CAA phenotypes, such as lobar hemorrhage, requires further investigation.