Project/Area Number |
15K15336
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Neurology
|
Research Institution | Kanazawa University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
濱口 毅 金沢大学, 附属病院, 講師 (70452109)
|
Co-Investigator(Renkei-kenkyūsha) |
ONO Kenjiro 昭和大学, 医学部, 教授 (70377381)
SAKAI Kenji 金沢大学, 附属病院, 助教 (00572306)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 脳アミロイドアンギオパチー / アミロイドβ蛋白 / 伝播 / 剖検脳 / アルツハイマー病 |
Outline of Final Research Achievements |
To examine a hypothesis that sporadic cerebral amyloid angiopathy (CAA) can be transmitted from humans to humans through CAA-specific amyloid β-protein (Aβ) strain, we performed transmission experiments to R1.40 APP transgenic mice with brain samples from patients with CAA without Alzheimer's disease (AD) (n = 3), AD with CAA (n = 3), AD without CAA (n = 3), and no AD/CAA (n = 3). Western blot of brains from the mice inoculated with the human brain samples presented with Aβ(n = 9)with Aβ40 (n = 3) or Aβ42 predominance (n = 6). Immunohistochemically, all the mice showed Aβ deposition in the brain with remarkable variations of Aβ42/Aβ40 ratios [Aβ42 immunoreactive areas (%)/Aβ40 immunoreactive areas (%)]. Severity of CAA correlated with Aβ40 immunoreactive areas (%). Study on correlations in the pattern of Aβ deposition between human and mouse brains is ongoing.
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