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lüll PET-detectable tau pathology correlates with long-term neuropsychiatric outcomes in patients with traumatic brain injury Takahata K; Kimura Y; Sahara N; Koga S; Shimada H; Ichise M; Saito F; Moriguchi S; Kitamura S; Kubota M; Umeda S; Niwa F; Mizushima J; Morimoto Y; Funayama M; Tabuchi H; Bieniek KF; Kawamura K; Zhang MR; Dickson DW; Mimura M; Kato M; Suhara T; Higuchi MBrain 2019[Oct]; 142 (10): 3265-3279Tau 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.|Adult[MESH]|Alzheimer Disease/pathology[MESH]|Brain Injuries, Traumatic/*diagnostic imaging/*pathology[MESH]|Brain/pathology[MESH]|Chronic Traumatic Encephalopathy/pathology[MESH]|Female[MESH]|Humans[MESH]|Male[MESH]|Mental Disorders/etiology/metabolism[MESH]|Middle Aged[MESH]|Positron-Emission Tomography/methods[MESH]|Psychotic Disorders/etiology/pathology[MESH]|Tauopathies/*diagnostic imaging/metabolism[MESH]|White Matter/pathology[MESH]|tau Proteins/metabolism[MESH] |