Functional analysis of CHRNA7, a candidate gene product for schizophrenia
| Project/Area Number |
21700415
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Waseda University |
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Principal Investigator |
SAWAMURA Naoya 早稲田大学, 理工学術院, 准教授 (40449351)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 精神・神経疾患の病態と治療 / 分子・細胞・神経生物学 |
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| Research Abstract |
The nicotinic acetylcholine receptors, key players in neuronal communication, convert neurotransmitter binding into membrane electrical depolarization. CHRNA7 is a type of the neuronal nicotinic receptor, thought to have association with Alzheimer's disease, because Aβ42 is reported binding to CHRNA7 protein with high affinity. Furthermore, the decline of senile plaques had been detected in mutant APP transgenic mice by blocking of CHRNA7. In order to figure out the starting mechanism of As aggregation, we investigate the interaction between CHRNA7 and As. We hypothesized that Aβ aggregation requires CHRNA7 as scaffold molecule and did several experiments to confirm this hypothestis.
We found out that As43 bound to CHRNA7 with higher affinity than As42 both in vitro and on extracellular membranes. Moreover, the decline of intracellular As42 has been detected by knocking down CHRNA7's expression. Thus, CHRNA7 might be scaffold molecule with As42 or As43 to form senile plaque, and we considered this might relate to AD profoundly.
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Report
(4 results)
Research Products
(6 results)
