Imperial College London
Alternate

ProfessorRogerGunn

Faculty of Medicine, Department of Brain Sciences

Emeritus Professor of Molecular Neuroimaging
 
 
 
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Contact

 

r.gunn

 
 
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Location

 

Burlington DanesHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Gorgoraptis:2019:10.1126/scitranslmed.aaw1993,
author = {Gorgoraptis, N and Li, LM and Whittington, A and Zimmerman, KA and Maclean, LM and McLeod, C and Ross, E and Heslegrave, A and Zetterberg, H and Passchier, J and Matthews, PM and Gunn, RN and McMillan, TM and Sharp, DJ},
doi = {10.1126/scitranslmed.aaw1993},
journal = {Science Translational Medicine},
pages = {1--14},
title = {In vivo detection of cerebral tau pathology in long-term survivors of traumatic brain injury},
url = {http://dx.doi.org/10.1126/scitranslmed.aaw1993},
volume = {11},
year = {2019}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - 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.
AU  - Gorgoraptis,N
AU  - Li,LM
AU  - Whittington,A
AU  - Zimmerman,KA
AU  - Maclean,LM
AU  - McLeod,C
AU  - Ross,E
AU  - Heslegrave,A
AU  - Zetterberg,H
AU  - Passchier,J
AU  - Matthews,PM
AU  - Gunn,RN
AU  - McMillan,TM
AU  - Sharp,DJ
DO  - 10.1126/scitranslmed.aaw1993
EP  - 14
PY  - 2019///
SN  - 1946-6234
SP  - 1
TI  - In vivo detection of cerebral tau pathology in long-term survivors of traumatic brain injury
T2  - Science Translational Medicine
UR  - http://dx.doi.org/10.1126/scitranslmed.aaw1993
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000484406300002&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://stm.sciencemag.org/content/11/508/eaaw1993
UR  - http://hdl.handle.net/10044/1/74002
VL  - 11
ER  -
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