| Project/Area Number |
25670425
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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 | Keio University |
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Principal Investigator |
ABE Yoichiro 慶應義塾大学, 医学部, 講師 (10317331)
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| Co-Investigator(Kenkyū-buntansha) |
NIIKURA Takako 上智大学, 理工学部, 准教授 (10301491)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | アルツハイマー病 / アストロサイト / ミクログリア / アクアポリン４ / マウスモデル / タウ / アミロイドβ / 遺伝子改変マウス / 疾患モデル |
|---|
| Outline of Final Research Achievements |
It has been suggested that progression of Alzheimer’s disease is enhanced by a lot of changes in environment inside the brain. Since it is well known that astrocytes have a role in maintaining brain environment, we focused on the effect of astrocytic dysfunction in Alzheimer’s model mice by disrupting their aquaporin-4 gene. Aquaporin-4 is a water channel in the brain expressed in astrocytes and has a role in water homeostasis in the brain. Although amyloid plaque formation and reactive astrocytosis surrounding the plaques were not altered, microgliosis around the plaques was significantly reduced in cortical area in the Alzheimer’s model lacking aquaporin-4.
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