Open AccessIn vivo coupling of tau pathology and cortical thinning in Alzheimer's disease
Author(s) -
Mak Elijah,
Bethlehem Richard A.I.,
RomeroGarcia Rafael,
Cervenka Simon,
Rittman Timothy,
Gabel Silvy,
Surendranathan Ajenthan,
BevanJones Richard W.,
Passamonti Luca,
Vázquez Rodríguez Patricia,
Su Li,
Arnold Robert,
Williams Guy B.,
Hong Young T.,
Fryer Tim D.,
Aigbirhio Franklin I.,
Rowe James B.,
O'Brien John T.
Publication year - 2018
Publication title -
alzheimer's and dementia: diagnosis, assessment and disease monitoring
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.497
H-Index - 37
ISSN - 2352-8729
DOI - 10.1016/j.dadm.2018.08.005
Subject(s) - atrophy , tau pathology , neuroscience , autopsy , pathology , alzheimer's disease , psychology , disease , medicine
The deposition of neurofibrillary tangles in neurodegenerative disorders is associated with neuronal loss on autopsy; however, their in vivo associations with atrophy across the continuum of Alzheimer's disease (AD) remain unclear. Methods We estimated cortical thickness, tau ([ 18 F]‐AV‐1451), and amyloid β (Aβ) status ([ 11 C]‐PiB) in 47 subjects who were stratified into Aβ− (14 healthy controls and six mild cognitive impairment–Aβ−) and Aβ+ (14 mild cognitive impairment–Aβ+ and 13 AD) groups. Results Compared with the Aβ− group, tau was increased in widespread regions whereas cortical thinning was restricted to the temporal cortices. Increased tau binding was associated with cortical thinning in each Aβ group. Locally, regional tau was associated with temporoparietal atrophy. Discussion These findings position tau as a promising therapeutic target. Further studies are needed to elucidate the casual relationships between tau pathology and trajectories of atrophy in AD.