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In vivo detection of cerebral tau pathology in long-term survivors of traumatic brain injury

Artikel i vetenskaplig tidskrift
Författare N. Gorgoraptis
L. M. Li
A. Whittington
K. A. Zimmerman
L. M. Maclean
C. McLeod
E. Ross
A. Heslegrave
Henrik Zetterberg
J. Passchier
P. M. Matthews
R. N. Gunn
T. M. McMillan
D. J. Sharp
Publicerad i Science Translational Medicine
Volym 11
Nummer/häfte 508
ISSN 1946-6234
Publiceringsår 2019
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Språk en
Länkar dx.doi.org/10.1126/scitranslmed.aaw...
Ämnesord positron-emission-tomography, amyloid-beta accumulation, voxel-based, morphometry, alzheimers-disease, cerebrospinal-fluid, head-injury, neuropathological criteria, cognitive impairment, hydrolase l1, mouse, model, Cell Biology, Research & Experimental Medicine
Ämneskategorier Neurovetenskaper

Sammanfattning

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) epsilon 4 genotype affected the relationship between flortaucipir binding and time since injury, CSF beta amyloid 1-42 (A beta 42) 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.

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