| Project/Area Number |
26893290
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Emergency medicine
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| Research Institution | Nippon Medical School |
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Principal Investigator |
YAMADA Marina 日本医科大学, 医学部, 講師 (70508621)
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| Research Collaborator |
MIYASHITA Masao 日本医科大学, 医学部, 教授 (70229847)
YOKOTA Hiroyuki 日本医科大学, 大学院医学研究科, 教授 (60182698)
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| Project Period (FY) |
2014-08-29 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 感染症 / 脳・神経障害 / 敗血症 / 行動薬理 / 脳・神経 / 認知機能障害 |
|---|
| Outline of Final Research Achievements |
Marked increase in survival after critical conditions, such as severe sepsis, have led us to further improve long-term illness described as post-intensive care syndrome (PICS), which covers both physical and psychiatric dysfunction among patients recovered from intensive care. The aim of the study was to elucidate the mechanisms underlying neuropsychiatric impairment in PICS. We developed murine PICS model by cecal ligation and puncture (CLP). CLP-induced sepsis caused acute increase in inflammatory cytokines and induced gliosis in the central nervous system, leading to working memory impairment in Y-maze. Administration of a neuroprotective peptide named humanin G (HNG) significantly suppressed acute inflammatory responses in CLP mice. HNG treatment, also, attenuated memory impairment, chronic loss of cholinergic neurons in the basal forebrain and decrease in synaptic plasticity of hippocampal neurons in CLP mice.
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