| Project/Area Number |
24500442
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | University of Miyazaki |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NEMOTO TAKAYUKI 宮崎大学, 医学部, 助教 (90506833)
MURAKAMI MANABU 弘前大学, 医学部, 教授 (80302090)
|
|---|
| Project Period (FY) |
2012-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | インスリン抵抗性 / インスリン受容体シグナル / 神経変性疾患 / 海馬神経細胞 / βアミロイド / 発現調節 / ネガティブフィードバック / 脳・神経 / インスリンシグナル / 神経保護作用 / インスリンシグナリング / ネガティブ フィードバッ ク / インスリン受容体 / ネガティブ フィードバック / 生理活性物質 |
|---|
| Outline of Final Research Achievements |
Dysregulated insulin receptor signaling (insulin resistance) may be involved in dementia and neurodegenerative disease (e.g. Alzheimer’s disease), thus insulin receptor signaling being the major molecular targets of neuroprotective drugs. In the present study, we have demonstrated that the insulin receptor signaling was up- and down-modulated by several therapeutic drugs and bioactive agents (e.g. nicotine, crucmin, immunosuppressants and alchol) via multiple intracellular mechanisms.
Synthesized insulin in rat hippocampal neurons is secreted by depolarization, and the activation of glycogen synthase kinase-3β in Amyloid β(1-42)-induced Alzheimer's model hippocampal neurons decreases the insulin synthesis.
|
