2015 Fiscal Year Final Research Report
Basic and translational research for protection of neurodegeneration.
Project/Area Number |
23249079
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Research Category |
Grant-in-Aid for Scientific Research (A)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Emergency medicine
|
Research Institution | Hoshi University (2015) Showa University |
Principal Investigator |
SHIODA SEIJI 星薬科大学, 付置研究所, 教授 (80102375)
|
Co-Investigator(Kenkyū-buntansha) |
Dohi Kenji 東京慈恵会医科大学, 医学部, 准教授 (20301509)
Nakamachi Tomoya 富山大学, 理工学研究部, 助教 (30433840)
Miyata Atsurou 鹿児島大学, 医学部, 教授 (60183969)
RAKWAL RANDEEP 筑波大学, 体育系, 教授 (70590850)
Hirokazu Otaki 昭和大学, 医学部, 講師 (20349062)
Satoshi Ikeda 鹿児島大学, 医学部, 講師 (00343369)
|
Project Period (FY) |
2011-04-01 – 2016-03-31
|
Keywords | PACAP / 神経細胞死防御 / ヒト骨髄間葉系幹細胞 / 神経損傷の防御 / トランスレーショナルリサーチ |
Outline of Final Research Achievements |
PACAP is expressed in neural tissues and is known to exert pleiotropic effects on the nervous system. Although its mechanisms of action are slowly being unraveled. This research was tried to demonstrate the neuroprotective effects, mechanisms, and therapeutic potential of PACAP using stroke and spinal injury model in mice. It appeared that PACAP inhibited delayed neuronal cells in brain and spinal cord and we found that PACAP affected on brain and spinal injury not only to inhibit neuronal cell death through MAPK signaling pathway but also it stimulated to activate and synthesize protein named CRMP2 which has been already reported to activate axonal cell growth in rodents utilizing high-throughout omics approaches. Moreover, we tried to make clear the functional significance of PACAP in primate, so we used common marmoset and we built up stroke model in them and we are now trying to test whether PACAP inhibits neural degeneration in humans in future.
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Free Research Field |
緊急医学
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