@misc{oai:repo.qst.go.jp:00065826,
 author = {Takahata, Keisuke and Shimada, Hitoshi and Higuchi, Makoto and Shinotoh, Hitoshi and Kimura, Yasuyuki and Kitamura, Soichiro and Endo, Hironobu and Niwa, Fumitoshi and Moriguchi, Sho and Ichise, Masanori and Sahara, Naruhiko and Mimura, Masaru and Kato, Motoichiro and Yamada, Makiko and Suhara, Tetsuya and Takahata, Keisuke and Shimada, Hitoshi and Higuchi, Makoto and Shinoto, Hitoshi and Kimura, Yasuyuki and Kitamura, Soichiro and Endo, Hironobu and Niwa, Fumitoshi and Moriguchi, Sho and Ichise, Masanori and Sahara, Naruhiko and Mimura, Masaru and Kato, Motoichiro and Yamada, Makiko and Suhara, Tetsuya},
 month = {May},
 note = {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},
 title = {Imaging of Tau and Amyloid Pathology in Patients with Traumatic Brain Injury: A PET Study Usinig [11C]PBB3 and [11C]PIB},
 year = {2015}
}