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

Gorgoraptis, N. (author)
Li, L. M. (author)
Whittington, A. (author)
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Zimmerman, K. A. (author)
Maclean, L. M. (author)
McLeod, C. (author)
Ross, E. (author)
Heslegrave, A. (author)
Zetterberg, Henrik, 1973 (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Passchier, J. (author)
Matthews, P. M. (author)
Gunn, R. N. (author)
McMillan, T. M. (author)
Sharp, D. J. (author)
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 (creator_code:org_t)
American Association for the Advancement of Science (AAAS), 2019
2019
English.
In: Science Translational Medicine. - : American Association for the Advancement of Science (AAAS). - 1946-6234 .- 1946-6242. ; 11:508
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Neurosciences (hsv//eng)

Keyword

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

Publication and Content Type

ref (subject category)
art (subject category)

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