In vivo detection of cerebral tau pathology in long-term survivors of traumatic brain injury
File(s)
Accepted version
Author(s)
Type
Journal Article
Abstract
Traumatic brain injury (TBI) can trigger progressive neurodegeneration, with tau pathology seen years after a single moderate-severe TBI. Identifying this type of posttraumatic pathology in vivo might help to understand the role of tau pathology in TBI pathophysiology. We used flortaucipir positron emission tomography (PET) to investigate whether tau pathology is present many years after a single TBI in humans. We examined PET data in relation to markers of neurodegeneration in the cerebrospinal fluid (CSF), structural magnetic resonance imaging measures, and cognitive performance. Cerebral flortaucipir binding was variable, with many participants with TBI showing increases in cortical and white matter regions. At the group level, flortaucipir binding was increased in the right occipital cortex in TBI when compared to healthy controls. Flortaucipir binding was associated with increased total tau, phosphorylated tau, and ubiquitin carboxyl-terminal hydrolase L1 CSF concentrations, as well as with reduced fractional anisotropy and white matter tissue density in TBI. Apolipoprotein E (APOE) ε4 genotype affected the relationship between flortaucipir binding and time since injury, CSF β amyloid 1–42 (Aβ42) concentration, white matter tissue density, and longitudinal Mini-Mental State Examination scores in TBI. The results demonstrate that tau PET is a promising approach to investigating progressive neurodegeneration associated with tauopathy after TBI.
Date Issued
2019-09-04
Date Acceptance
2019-08-02
Citation
Science Translational Medicine, 2019, 11 (508), pp.1-14
ISSN
1946-6234
Publisher
American Association for the Advancement of Science
Start Page
1
End Page
14
Journal / Book Title
Science Translational Medicine
Volume
11
Issue
508
Copyright Statement
© 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works http://www.sciencemag.org/about/science-licenses-journal-article-reuseThis is an article distributed under the terms of the Science Journals Default License.
Identifier
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000484406300002&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
Subjects
Science & Technology
Life Sciences & Biomedicine
Cell Biology
Medicine, Research & Experimental
Research & Experimental Medicine
POSITRON-EMISSION-TOMOGRAPHY
AMYLOID-BETA ACCUMULATION
VOXEL-BASED MORPHOMETRY
ALZHEIMERS-DISEASE
CEREBROSPINAL-FLUID
HEAD-INJURY
NEUROPATHOLOGICAL CRITERIA
COGNITIVE IMPAIRMENT
HYDROLASE L1
MOUSE MODEL
Publication Status
Published
Article Number
eaaw1993
Date Publish Online
2019-09-04