The role of prostanoid receptor CRTH2 on the emotional dysfunction lasting after cancer treatment
Project/Area Number |
17K15461
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Pharmacology in pharmacy
|
Research Institution | Setsunan University |
Principal Investigator |
Onaka Yusuke 摂南大学, 薬学部, 講師 (90749003)
|
Research Collaborator |
HASHIMOTO HITOSHI
SHINTANI NORIHITO
NAKAZAWA TAKANOBU
AGO YUKIO
OGITA KIYOKAZU
YONEYAMA MASANORI
YAMAGUCHI TARO
|
Project Period (FY) |
2017-04-01 – 2019-03-31
|
Project Status |
Completed (Fiscal Year 2018)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | CRTH2 / プロスタグランジン / がん / 精神機能障害 / 行動薬理学 / 薬学 / 脳・神経 / 薬理学 / 行動解析 / 癌 |
Outline of Final Research Achievements |
Recently, it has been reported that cancer-related brain dysfunctions would last for a long time after the completion of treatment. This study revealed that depression-like behavior, which was seen in tumor-resected mice, might be mediated by a hippocampal prostanoid signaling via CRTH2 receptor in mice. The present study also found that microglial dysfunction was caused in the hippocampus of tumor-resected mice. These data suggest that the treatment which targets hippocampal specific signaling could be an efficacious strategy.
|
Academic Significance and Societal Importance of the Research Achievements |
がん患者では、抑うつ症状や注意力の低下などの精神機能障害が認められることがあり、一部のがん患者では、治療の終了後も、これらの障害が長期的に認められる場合がある。しかし、そのメカニズムの詳細は不明であった。本研究では、腫瘍の形成とその切除により引き起こされる精神機能障害のメカニズムの一端に、海馬の機能異常が関与する可能性を明らかにした。腫瘍の切除後において認められる海馬の機能異常を標的とした治療を行うことで、がん治療後に持続する精神機能障害の緩和につながることが期待される。
|
Report
(3 results)
Research Products
(36 results)