Presentation Imaging of Tau and Amyloid Pathology in Patients with Traumatic Brain Injury: A PET Study Usinig [11C]PBB3 and [11C]PIB

Takahata, Keisuke  ,  Shimada, Hitoshi  ,  Higuchi, Makoto  ,  Shinotoh, Hitoshi  ,  Kimura, Yasuyuki  ,  Kitamura, Soichiro  ,  Endo, Hironobu  ,  Niwa, Fumitoshi  ,  Moriguchi, Sho  ,  Ichise, Masanori  ,  Sahara, Naruhiko  ,  Mimura, Masaru  ,  Kato, Motoichiro  ,  Yamada, Makiko  ,  Suhara, Tetsuya

Backgrounds: Chronic traumatic encephalopathy (CTE) is a delayed-onset neurodegenerative disease, which occurs several years after traumatic brain injury (TBI). Pathologically, CTE is characterized by abnormal accumulations including tau changes, amyloid-beta proteins. Using a novel tau ligand [11C]PBB3 and amyloid ligand [11C]PIB, we explored in vivo imaging of tau and amyloid pathology in TBI patients.Methods: Three patients with repetitive mild TBI (2 wrestlers, 1 kick boxer), two patients with single severe TBI (1 diffuse axonal injury, 1 acute subdural hematoma) and 20 age-matched healthy controls (HCs) underwent MRI and PET scans using [11C]PBB3 and [11C]PIB. For each PET data, standardized uptake value ratio (SUVR) using cerebellum as a reference region was calculated. Amyloid deposition was evaluated by visual assessment of SUVR images of [11C]PIB PET. Tau deposition was evaluated by visual assessment and VOI analysis of SUVR images of [11C]PBB3 PET. Cognitive impairments were also evaluated with neuropsychological tests.Results: In HCs, none was [11C]PBB3- or [11C]PIB-positive. In TBI patients, memory impairment was the most frequent symptom. All TBI patients were [11C]PIB-negative, indicating absence of amyloid beta deposition. In contrast, four of five TBI patients showed high [11C]PBB3 binding in the medial temporal cortex. High [11C]PBB3 binding was also observed in the insular and the frontal cortex. Some of these [11C]PBB3-binding regions exhibited local cortical atrophy. Cortical atrophy was present in some of these regions.Conclusions: These preliminary findings provided the evidence of TBI-induced tau pathology consistent with postmortem studies.
Annual Meeting of Society of Biological Psychiatry

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