2017 Fiscal Year Final Research Report
Study on transmission of sporadic cerebral amyloid angiopathy
| Project/Area Number |
15K15336
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurology
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
濱口 毅 金沢大学, 附属病院, 講師 (70452109)
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| 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)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| 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 |
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| 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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| Free Research Field |
神経内科学
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