The cortical origin and initial spread of medial temporal tauopathy in Alzheimer’s disease assessed with positron emission tomography
Justin S. Sanchez(Harvard University), J. Alex Becker(Harvard University), Heidi I.L. Jacobs(Harvard University), Bernard Hanseeuw(Harvard University), Shu Jiang(Harvard University), Aaron P. Schultz(Harvard University), Michael J Properzi(Harvard University), Samantha Katz(Harvard University), Alexa Beiser(Boston University), Claudia L. Satizábal(Boston University), Adrienne O’Donnell(Boston University), Charles DeCarli(University of California, Davis), Ronald Killiany(Boston University), Georges El Fakhri(Harvard University), Marc D. Normandin(Harvard University), Teresa Gómez‐Isla(Harvard University), Yakeel T. Quiroz(Harvard University), Dorene M. Rentz(Brigham and Women's Hospital), Reisa A. Sperling(Brigham and Women's Hospital), Sudha Seshadri(Boston University), Jean C. Augustinack(Harvard University), Julie C. Price(Harvard University), Keith A. Johnson(Brigham and Women's Hospital)
Cited by 206Open Access
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.
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