2016 Fiscal Year Final Research Report
Investigating the mechanisms of stress-induced depression via neuroinflammation and development of the new strategy for the treatment of depression.
Project/Area Number |
15K19729
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Psychiatric science
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Research Institution | Tottori University |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2017-03-31
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Keywords | うつ病 / ストレス / 炎症 / サイトカイン / NLRP3 / IL-1β / TNFα |
Outline of Final Research Achievements |
We revealed that i) stress, which plays a critical role in the onset of depression, causes neuroinflammation via the innate immune system in the brain, and that ii) the key molecule which senses stress is a cytosolic pattern recognition receptor called NLRP3. We also demonstrated that beta-hydroxybutyrate (BHB), an endogenic NLRP3 inflammasome inhibitor, showed the antidepressant effects in a rodent model of chronic unpredictable stress, and that BHB attenuated the increased levels of IL-1β in the hippocampus by stress. These findings demonstrate that BHB exerts antidepressant-like effects, possibly by inhibiting NLRP3-induced neuro-inflammation in the hippocampus, and that BHB may be a novel therapeutic candidate for the treatment of stress-related mood disorders.
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Free Research Field |
うつ病
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