2016 Fiscal Year Final Research Report
Tau deposition and microglial activation, amyroid deposition Alzheimer disease
Project/Area Number |
15K19481
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Neurology
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Research Institution | National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders |
Principal Investigator |
Terada Tatsuhiro 独立行政法人国立病院機構(静岡・てんかん神経医療センター臨床研究部), 神経内科, その他 (80550178)
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Project Period (FY) |
2015-04-01 – 2017-03-31
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Keywords | アルツハイマー病 / タウ / ミクログリア / アミロイド / PET / PBB3 |
Outline of Final Research Achievements |
Amyloid-beta and tau are representative proteins that characterize the pathology of Alzheimer’s disease (AD). It remains unclear whether tau pathology and neuroinflammation occur in parallel. Tau and activated microglia can be depicted in vivo with a newly developed positron emission tomography (PET) tracers [11C]PBB3 and [11C]DPA713, respectively.AD patient at the CDR0.5 exhibited [11C]PBB3 BPND increase in the temporal and frontal cortex. In contrast, AD patient at the CDR1 showed greater elevation of [11C]PBB3 BPND more broadly in the temporal, parietal, and frontal cortices. In the right hippocampus, positive correlation was found between [11C]PBB3 BPND and [11C]DPA713 BPND.In addition, thre were significant correlation between increased [11C]PBB3 in the temporal area and amyroid deposition in the frontal area. Our results were consistent with tau spreading known in the AD pathology, and tau deposition may accompany microglial activation in the cerebral cortex.
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Free Research Field |
神経内科学
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