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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.

Research Project

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Project/Area Number 15K19729
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Psychiatric science
Research InstitutionTottori University

Principal Investigator

Iwata Masaaki  鳥取大学, 医学部, 准教授 (40346367)

Project Period (FY) 2015-04-01 – 2017-03-31
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.

Free Research Field

うつ病

URL: 

Published: 2018-03-22  

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