The cortical origin and initial spread of medial temporal tauopathy in Alzheimer’s disease assessed with positron emission tomography
Justin S. Sanchez, J. Alex Becker, Heidi I.L. Jacobs, Bernard Hanseeuw, Shu Jiang, Aaron P. Schultz, Michael J Properzi, Samantha Katz, Alexa Beiser, Claudia L. Satizábal, Adrienne O’Donnell, Charles DeCarli, Ronald Killiany, Georges El Fakhri, Marc D. Normandin, Teresa Gómez‐Isla, Yakeel T. Quiroz, Dorene M. Rentz, Reisa A. Sperling, Sudha Seshadri, Jean C. Augustinack, Julie C. Price, Keith A. Johnson
Abstract
= 104), tracked Aβ-associated spread of TAU from this site first to nearby neocortex of the temporal lobe and then to extratemporal regions. Greater rate of TAU spread was associated with baseline measures of both global Aβ burden and medial temporal lobe TAU. These findings are consistent with clinicopathological correlation studies of Alzheimer's tauopathy and enable precise tracking of AD-related TAU progression for natural history studies and prevention therapeutic trials.