| Project/Area Number |
18K16247
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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| Research Institution | Aichi Medical University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 糖尿病性神経障害 / Diabetic polyneuropathy / Notch signaling / 糖尿病性多発神経障害 / 糖尿病性合併症 / 糖尿病神経障害 / Notch / 神経幹細胞 |
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| Outline of Final Research Achievements |
The mechanisms of diabetic polyneuropathy (DPN) are not fully understood. In this study, to examine whether regenerative and homeostatic mechanisms are involved in the pathogenesis of DPN, we focused on the interaction between abnormal insulin signaling and Notch signaling, which is an important pathway to keep static phase of neural stem cells/progenitor cells (NSC/NPC).
As a result, we confirmed that insulin signaling is enhanced and Notch signaling is suppressed in the peripheral nervous system of diabetic mice. Furthermore, NSC/NPC is reduced at the early stage of the life in these mice. We confirmed axonal degeneration of peripheral nerves in mice lacking peripheral nervous system-specific insulin-Notch signaling. These results suggest that quantitative changes in NSC/NPC are involved in DPN.
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| Academic Significance and Societal Importance of the Research Achievements |
糖尿病性多発神経障害は高頻度な糖尿病性合併症である。本研究では糖尿病性多発神経障害の病態の一部を解明した。
糖尿病性多発神経障害は病態の解明が不十分であるため、治療法の開発も停滞している状況である。このような状況において、本研究の成果を応用することで、今後、この疾患に対する治療法の開発が進むことが期待できる。
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