2016 Fiscal Year Final Research Report
Elucidation of mechanisms of the development of auditory and balance disorders associated with aging and establishment of the treatment strategy against them
| Project/Area Number |
26253081
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
岩崎 真一 東京大学, 医学部附属病院, 准教授 (10359606)
樫尾 明憲 東京大学, 医学部附属病院, 助教 (20451809)
柿木 章伸 東京大学, 医学部附属病院, 准教授 (60243820)
藤本 千里 東京大学, 医学部附属病院, 助教 (60581882)
松本 有 東京大学, 医学部附属病院, 助教 (80548553)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 神経科学 / 老化 / 難聴 / 酸化ストレス / ミトコンドリア |
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| Outline of Final Research Achievements |
When endogenous antioxidant MnSOD was reduced to half, oxidation stress of the cochlea was exacerbated by aging and acoustic trauma aggravated it. When GeO2 was given to mice, cochlear tissue showed marked degeneration with decrease of mitochondrial function. This damage was ameliorated by antioxidant. When gentamycin was injected into the middle ear, hair cell(HC) in semicircular canal showed marked degeneration and showed partial recovery due to regeneration via cell division of the sopporting cells. When TrkB agonist was given, HC showed significant recovery and synapse and afferent fibers were better preserved. When immortalized inner ear cells were exposed to oxidation stress, mitochondria were degenerated, mitochondrial membrane potential decreased, mitochondrial fusion/fission was impaired, and respiratory capacity was affected. We found that the cochlear HC, possess autophagy functoion. When Atg5 was knock out in the cochlear HC, these cells exhibited progressive degeneration.
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| Free Research Field |
耳鼻咽喉科学
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