量研学術機関リポジトリ「QST-Repository」は、国立研究開発法人 量子科学技術研究開発機構に所属する職員等が生み出した学術成果（学会誌発表論文、学会発表、研究開発報告書、特許等）を集積しインターネット上で広く公開するサービスです。 Welcome to QST-Repository where we accumulates and discloses the academic research results(Journal Publications, Conference presentation, Research and Development Report, Patent, etc.) of the members of National Institutes for Quantum Science and Technology.
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Tau deposits is a core feature of neurodegenerative disorder following traumatic brain injury (TBI). Despite ample evidence from
post-mortem studies demonstrating exposure to both mild-repetitive and severe TBIs are linked to tau depositions, associations of
topology of tau lesions with late-onset psychiatric symptoms due to TBI have not been explored. To address this issue, we assessed
tau deposits in long-term survivors of TBI by PET with 11C-PBB3, and evaluated those associations with late-life neuropsychiatric
outcomes. PET data were acquired from 27 subjects in the chronic stage following mild-repetitive or severe TBI and 15 healthy
control subjects. Among the TBI patients, 14 were diagnosed as having late-onset symptoms based on the criteria of traumatic
encephalopathy syndrome. For quantification of tau burden in TBI brains, we calculated 11C-PBB3 binding capacity (cm3), which
is a summed voxel value of binding potentials (BP*
ND) multiplied by voxel volume. Main outcomes of the present study were
differences in 11C-PBB3 binding capacity between groups, and the association of regional 11C-PBB3 binding capacity with neuropsychiatric
symptoms. To confirm 11C-PBB3 binding to tau deposits in TBI brains, we conducted in vitro PBB3 fluorescence and
phospho-tau antibody immunofluorescence labelling of brain sections of chronic traumatic encephalopathy obtained from the
Brain Bank. Our results showed that patients with TBI had higher 11C-PBB3 binding capacities in the neocortical grey and
white matter segments than healthy control subjects. Furthermore, TBI patients with traumatic encephalopathy syndrome
showed higher 11C-PBB3 binding capacity in the white matter segment than those without traumatic encephalopathy syndrome,
and regional assessments revealed that subgroup difference was also significant in the frontal white matter. 11C-PBB3 binding
capacity in the white matter segment correlated with the severity of psychosis. In vitro assays demonstrated PBB3-positive tau
inclusions at the depth of neocortical sulci, confirming 11C-PBB3 binding to tau lesions. In conclusion, increased 11C-PBB3 binding
capacity is associated with late-onset neuropsychiatric symptoms following TBI, and a close correlation was found between
psychosis and 11C-PBB3 binding capacity in the white matter
PET-detectable tau pathology correlates with long-term neuropsychiatric outcomes in patients with traumatic brain injury
