| Project/Area Number |
21800016
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Tokyo University of Technology (2010)
Tokyo Medical and Dental University (2009) |
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Principal Investigator |
SUZUKI Ikuro Tokyo University of Technology, 応用生物学部, 助教 (90516311)
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| Project Period (FY) |
2009 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥2,652,000 (Direct Cost: ¥2,040,000、Indirect Cost: ¥612,000)
Fiscal Year 2010: ¥1,261,000 (Direct Cost: ¥970,000、Indirect Cost: ¥291,000)
Fiscal Year 2009: ¥1,391,000 (Direct Cost: ¥1,070,000、Indirect Cost: ¥321,000)
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| Keywords | 神経細胞 / アミロイドβ / 多電極アレイ / 時系列解析 / チモキノン / 長期計測 / DFA / アルツハイマー病 / 脳・神経 / 自発活動 / 海馬神経細胞 / 生物物理 |
|---|
| Research Abstract |
Alzheimer's disease (AD) is characterized by the aggregation of amyloid β peptide (Aβ). The aim of this study is to investigate the effect of Amyloid Beta toxicity in embryonic rat hippocampus through chronic monitoring of neuronal cell electrical activity using multielectrode array (MEA) recordings, and the molecules protecting neurons from Aβ toxicity. Applying Aβ to cultured embryonic rat hippocampal neurons has an inhibitory effect on spontaneous activity started 24h after applying and the firing disappeared at 72h. When thymoquinone (TQ) active constituent of Nigella Sativa Oil and Aβ were simultaneously applied, thymoquinone reduces the deleterious effect of Aβ at 34h after applying. This results indicated that TQ have the potential protecting hippocampus cells from Aβ toxicity.
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