| Project/Area Number |
18K15444
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 52020:Neurology-related
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 高速原子間力顕微鏡 / アミロイドβ蛋白 / 凝集 / 脳実質 / 脳血管 / 凝集過程 / amyloid β |
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| Outline of Final Research Achievements |
To examine a hypothesis that a diversity of amyloid beta protein (Abeta) deposition and clinical and pathological features of Alzheimer's disease (AD) were associated with different features of Abeta aggregation and structural forms, we analyzed Abeta aggregation using thioflavin T (ThT) assay, electron microscopy (EM), and high-speed atomic force microscopy (HS-AFM). Abeta aggregation was accelerated when Abeta monomer were incubated with Abeta seeds. EM images demonstrated non-branched fibrillar structures of Abeta1-40 and Abeta1-42 aggregates. Three structural types of Abeta1-42 fibrils were identified during observation in HS-AFM.
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| Academic Significance and Societal Importance of the Research Achievements |
アミロイドβ蛋白 (amyloid β protein: Aβ) は、主に脳実質と血管壁に沈着する。孤発性Alzheimer病（孤発性AD）には、脳実質の老人斑が主体で、典型的なADの臨床病理像を呈するものや血管壁に高度のcerebral amyloid angiopathy (CAA) を認め、脳出血を頻回に起こすものなど、臨床病理像に多様性があることが知られている。また、遺伝性ADの原因遺伝子の1つであるAPP遺伝子変異の種類によっても脳実質のAβ沈着が主体のもの、血管壁のAβ沈着が主体のものなど、異なった臨床病理像をとることが知られているが、詳細についてはわかっていない。
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