| 研究課題/領域番号 |
23K14675
|
|---|
| 研究種目 |
若手研究
|
| 配分区分 | 基金 |
|---|
| 審査区分 |
小区分51010:基盤脳科学関連
|
|---|
| 研究機関 | 順天堂大学 |
|---|
研究代表者 |
COSSU DAVIDE 順天堂大学, 健康総合科学先端研究機構, 准教授 (90867326)
|
|---|
| 研究期間 (年度) |
2023-04-01 – 2026-03-31
|
| 研究課題ステータス |
交付 (2023年度)
|
| 配分額 *注記 |
4,680千円 (直接経費: 3,600千円、間接経費: 1,080千円)
2025年度: 780千円 (直接経費: 600千円、間接経費: 180千円)
2024年度: 2,080千円 (直接経費: 1,600千円、間接経費: 480千円)
2023年度: 1,820千円 (直接経費: 1,400千円、間接経費: 420千円)
|
|---|
| キーワード | mitochondria / neuroinflammation / Epstein barr virus / endogenous retrovirus / mycobacteria / multiple sclerosis / parkinson'disease / immunity / mitophagy / infection / EAE |
|---|
| 研究開始時の研究の概要 |
To investigate the relationships between mitophagy, infections and neuroinflammation, the project is divided into different phases: 1) microbial identification in patients, 2) gene expression analysis in patients, 3) development of animal models to study the effect of mitophagy and infections.
|
| 研究実績の概要 |
We discovered a significant correlation between antibodies targeting Epstein Barr virus (EBV) and human endogenous retrovirus (HERV-W) peptides among a specific subset of Multiple Sclerosis (MS) patients. These findings underscore EBV's involvement in MS pathogenesis, indicating its potential to trigger HERV-W reactivation. Furthermore, our research presents compelling evidence linking Mycobacterium paratuberculosis to the onset or worsening of MS, particularly in a subgroup of patients exhibiting elevated serum IgG4 levels. Additionally, we devised an alternative approach to induce Experimental Autoimmune Encephalomyelitis using heat-killed mycobacterium. Lastly, we uncovered a crucial role played by the immune system and mitochondrial dysfunction in Parkinson's disease.
|
| 現在までの達成度 (区分) |
現在までの達成度 (区分)
1: 当初の計画以上に進展している
理由
We're uncovering novel antigens from various pathogens that may play a role in neuroinflammation. Antibodies targeting these pathogens could serve as valuable markers for tracking disease progression in multiple sclerosis and other inflammatory disorders. Furthermore, these antigens seem to induce encephalitogenic effects in vivo, particularly in mice lacking mitophagy-related genes.
|
| 今後の研究の推進方策 |
To delve into the role of specific immunogenic antigens observed in patients with MS, NMOSD, and MOGAD, we propose immunizing knockout mice exhibiting mitochondrial abnormalities. This will be accomplished through two primary methods: inducing active experimental autoimmune encephalomyelitis (EAE) or utilizing the cuprizone model.
|
