• Keith A Johnson, Aaron Schultz, Rebecca A Betensky, J Alex Becker, Jorge Sepulcre, Dorene Rentz, Elizabeth Mormino, Jasmeer Chhatwal, Rebecca Amariglio, Kate Papp, Gad Marshall, Mark Albers, Samantha Mauro, Lesley Pepin, Jonathan Alverio, Kelly Judge, Marlie Philiossaint, Timothy Shoup, Daniel Yokell, Bradford Dickerson, Teresa Gomez-Isla, Bradley Hyman, Neil Vasdev, and Reisa Sperling.
• Division of Nuclear Medicine and Molecular Imaging, Boston, MA.
• Ann. Neurol. 2016 Jan 1; 79 (1): 110-9.

ObjectiveDetection of focal brain tau deposition during life could greatly facilitate accurate diagnosis of Alzheimer disease (AD), staging and monitoring of disease progression, and development of disease-modifying therapies.MethodsWe acquired tau positron emission tomography (PET) using (18)F T807 (AV1451), and amyloid-β PET using (11)C Pittsburgh compound B (PiB) in older clinically normal individuals, and symptomatic patients with mild cognitive impairment or mild AD dementia.ResultsWe found abnormally high cortical (18)F T807 binding in patients with mild cognitive impairment and AD dementia compared to clinically normal controls. Consistent with the neuropathology literature, the presence of elevated neocortical (18)F T807 binding particularly in the inferior temporal gyrus was associated with clinical impairment. The association of cognitive impairment was stronger with inferior temporal (18)F T807 than with mean cortical (11)C PIB. Regional (18)F T807 was correlated with mean cortical (11)C PiB among both impaired and control subjects.InterpretationThese findings suggest that (18)F T807 PET could have value as a biomarker that reflects both the progression of AD tauopathy and the emergence of clinical impairment.© 2015 American Neurological Association.

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