Widespread distribution of tauopathy in preclinical Alzheimer’s disease

Stephanie A. Schultz, Brian A. Gordon, Shruti Mishra, Yi Su, Richard J. Perrin, Nigel J. Cairns, John C. Morris, Beau M. Ances, Tammie L.S. Benzinger. Neurobiology of Aging, Volume 72, December 2018, Pages 177-185 Read More


The objective of this study was to examine the distribution and severity of tau-PET binding in cognitively normal adults with preclinical Alzheimer’s disease as determined by positive beta-amyloid PET. 18F-AV-1451 tau-PET data from 109 cognitively normal older adults were processed with 34 cortical and 9 subcortical FreeSurfer regions and averaged across both hemispheres. Individuals were classified as being beta-amyloid positive (N = 25, A+) or negative (N = 84, A−) based on a 18F-AV-45 beta-amyloid-PET standardized uptake value ratio of 1.22. We compared the tau-PET binding in the 2 groups using covariate-adjusted linear regressions. The A+ cohort had higher tau-PET binding within 8 regions: precuneus, amygdala, banks of the superior temporal sulcus, entorhinal cortex, fusiform gyrus, inferior parietal cortex, inferior temporal cortex, and middle temporal cortex. These findings, consistent with preclinical involvement of the medial temporal lobe and parietal lobe and association regions by tauopathy, emphasize that therapies targeting tauopathy in Alzheimer’s disease could be considered before the onset of symptoms to prevent or ameliorate cognitive decline. © 2018

Full Text


Posted on October 16, 2018
Posted in: HPAN, Neurodegeneration, Publications Authors: , , ,