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Sci Transl Med. 2019 Sep 4;11(508). pii: eaaw1993. doi: 10.1126/scitranslmed.aaw1993.

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

Author information

1
Department of Brain Sciences, Imperial College London, London W12 0NN, UK.
2
Invicro London, London W12 0NN, UK.
3
Institute of Health and Wellbeing, University of Glasgow, Glasgow G12 0XH, UK.
4
UK Dementia Research Institute, University College London, London WC1N 3BG, UK.
5
Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK.
6
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal 431 80, Sweden.
7
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal 413 45, Sweden.
8
UK Dementia Research Institute, Imperial College London, London W12 0NN, UK.
9
Department of Brain Sciences, Imperial College London, London W12 0NN, UK. david.sharp@imperial.ac.uk.

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.

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