2014 Fiscal Year Final Research Report
Exploration of analgesic target for tumor-induced neuropathic pain based on the molecular mechanism of circadian rhythm in allodynia
Project/Area Number |
24390149
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Pain science
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Research Institution | Kyushu University |
Principal Investigator |
KOYANAGI Satoru 九州大学, 薬学研究科(研究院), 准教授 (60330932)
|
Co-Investigator(Renkei-kenkyūsha) |
TSUDA Makoto 九州大学, 大学院薬学研究院, 教授 (40373394)
MATSUNAGA Naoya 九州大学, 大学院薬学研究院, 助教 (10432915)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | 神経障害痛 / 概日時計 / 医薬品開発 |
Outline of Final Research Achievements |
Pain in cancer is often associated with tumor compression or infiltration on tissues. Cancer-related neuropathic pain also arises from injury attributable to infiltration of malignant cells into peripheral nerves. One troublesome hallmark symptom of neuropathic pain is hypersensitivity to normally innocuous stimuli, a condition known as “tactile allodynia” that is refractory even to opioids. The intensity of neuropathic pain in patients with cancer has been known to vary over 24 hour. We aimed to clarify the molecular link connecting the circadian clock to neuropathic pain, and identified a molecule responsible for causing the circadian variation of “allodynia”. Importantly, suppressing the function of the circadian-allodynic molecule resulted in the significant attenuation of neuropathic pain. Identification of mechanism underlying the circadian change in the pathological condition will be useful strategy to discover new therapeutic target.
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Free Research Field |
疼痛学
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