| Project/Area Number |
26640005
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Neurophysiology / General neuroscience
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
Sanada Kamon 東京大学, 大学院理学系研究科(理学部), 准教授 (50431896)
|
|---|
| Research Collaborator |
KURABAYASHI Nobuhiro
IMAIZUMI Keisuke
TAMAI So-ichi
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 神経保護 / 概日時計 / 神経変性疾患 / 筋萎縮性側索硬化症 |
|---|
| Outline of Final Research Achievements |
ALS is a fatal and untreatable neurodegenerative disease characterized by the loss of upper and lower motor neurons. As enhancement of defense mechanisms intrinsic to neurons remains a potential strategy to counteract neuron degeneration in ALS, uncovering novel neuroprotective molecules within neurons could lead to the development of therapeutic approaches for ALS and related neurodegenerative diseases. We have previously found that NFIL3 (nuclear factor interleukin 3-regulated; also known as E4BP4) plays neuroprotective roles in neurons in vitro and in vivo. As NFIL3 is known to play important roles in the circadian clock system, particularly in the transcriptional control of clock gene periods, this raises potential roles of clock genes in neuroprotection. In the present study, we have found that Period2 protein levels control neuroprotective potential of neurons. The present study sheds light on a potential linkage between circadian clock proteins and neuroprotection.
|
