2017 Fiscal Year Final Research Report
Pathophysiological study of diabetes-related dementia
Project/Area Number |
15K09362
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurology
|
Research Institution | Tokyo Medical University |
Principal Investigator |
Hanyu Haruo 東京医科大学, 医学部, 教授 (10228520)
|
Co-Investigator(Kenkyū-buntansha) |
石井 賢二 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), 東京都健康長寿医療センター研究所, 研究部長 (10231135)
清水 聰一郎 東京医科大学, 医学部, 講師 (10385031)
櫻井 博文 東京医科大学, 医学部, 教授 (60235223)
松岡 正明 東京医科大学, 医学部, 主任教授 (70222297)
金高 秀和 東京医科大学, 医学部, 講師 (90385021)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Keywords | 認知症 / 糖尿病 / アミロイド / タウ / アルツハイマー病 |
Outline of Final Research Achievements |
We studied 11C-PiB (amyloid) and 11C-PBB3 (tau) positron emission tomography (PET) in 31 subjects with diabetes-related dementia (DrD). Depending on the positivity of PiB and PBB3, we classified 21 subjects into a negative PiB and a positive PBB3 pattern (11 cases, 52%), indicating tauopathy, a positive PiB and a positive PBB3 pattern (6 cases, 29%), indicating AD pathology, or a negative PiB and a negative PBB3 pattern (4 cases, 19%). Among 11 subjects showing a negative PiB and a positive PBB3 pattern, there were 2 PBB3 deposits patterns, including the medial temporal lobe only and extensive neocortex beyond the medial temporal lobe. DrD may be associated predominantly with tau pathology, in addition to Alzheimer pathology and non-amyloid/non-tau neuronal damage due to diabetes-related metabolic abnormalities.
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Free Research Field |
老年医学
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