2015 Fiscal Year Final Research Report
Insulin resistance in neurons: identification of the improving or worsening factors and their intracellular mechanisms
| 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
|
| 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 |
|---|
| 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.
|
| Free Research Field |
薬理学 神経科学
|
