1997 Fiscal Year Final Research Report Summary
Cell Biotechnology and Molecular Biology of Presbyacusis-related Gene and Its Clinical Application
| Project/Area Number |
08407054
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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 | Tohoku University |
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Principal Investigator |
TAKASAKA Tomonori Tohoku University, Medical School, Professor, 医学部, 教授 (80004646)
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| Co-Investigator(Kenkyū-buntansha) |
OSHIMA Takeshi Tohoku University, Medical School, Lecturer, 医学部, 助子 (40241608)
KAWASE Tetsuaki Tohoku University, Medical School, Assistant Professor, 医学部・附属病院, 講師 (50169728)
IKEDA Katsuhisa Tohoku University, Medical School, Assistant Professor, 医学部, 講師 (70159614)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Presbyacusis / Mitochondrial DNA / Aged mouse / DNA mutation / Hearing loss / RT-PCR / Digital hearing aid |
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| Research Abstract |
The inner ear composed of a post-mitotic stable tissue is a target organ for mitochondrial DNA (mtDNA) mutation. To determine whether mtDNA mutation is a predisposing factor in patients with sensorineural hearing loss (SNHL), we assessed the mtDNA^<4977> deletion from 60 patients with sensorineural hearing loss (SNHL) and 47 normal controls. All cases had no past history of ototoxic or noise exposure, middle ear disease, or other known etiological factors for SNHL.DNA specmiens extracted from peripheral blood leukocytes were used for detection of mtDNA^<4977> deletion by polymerase chain reaction. Patients with SNHL had a significantly high rate of the mtDNA^<4977> deletion than those of controls (75% vs 30%, p<0.0001). The detection rate of mtDNA^<4977> delection was significantly increased with the deterioration of the hearing threshold. Aging did not influence the detection rate of mtDNA^<4977> deletion in either the control or SNHL group. We have described high detection rates of the mtDNA^<4977> deletion in patients with idiopathic bilateral SNHL and propose that (at least) some of the advanced SNHL cases should be categorized as mitochondrial oxidative phosphorylation diseases. The present inference would offer novel possibilities for treatment and prevention of SNHL including presbycusis.
A mutant mitochondrial DNA (mtDNA) was investigated in the aged cochlea of the animal model of presbycusis. The aged mice showed a significant deterioration of hearing compared with the young mice. The mtDNA with a 4802 bp deletion was highly detected in the aged cochlea (80%) whereas no mtDNA deletion was recognized in the young mice. These results indicates that the mtDNA deletion contributes to pathophysiological processes underlying presbycusis.
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