| Project/Area Number |
16K08613
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | Osaka University (2017-2018)
The University of Tokyo (2016) |
|---|
Principal Investigator |
Kuma Akiko 大阪大学, 医学系研究科, 特任准教授(常勤) (30392377)
|
|---|
| Project Period (FY) |
2016-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | オートファジー / 選択的基質 / 神経変性疾患 / 神経疾患 |
|---|
| Outline of Final Research Achievements |
Autophagy is a degradation system within a cell. In this process, small portion of cytoplasmic components are engulfed by autophagosomes, transported to lysosomes and degraded. It has been reported that autophagy-deficient mice show phenotypes similar to neurodegenerative diseases. In order to clarify the cause, we performed MS analysis of the autophagy-deficient mouse brain and found that substrates, regulators and receptors for autophagy are highly accumulated. We focused on some of them, and we are in process of analyzing their role in autophagy and the relationship with the pathological condition in detail.
|
| Academic Significance and Societal Importance of the Research Achievements |
オートファジーは、アルツハイマーやパーキンソン病などの神経変性疾患との関連が強く示唆されており、脳におけるオートファジーの生理機能およびその破綻による神経症状の発症機序を理解することは、基礎生物学的にも医学的にも重要である。
|
