1999 Fiscal Year Final Research Report Summary
Clinical and cell biological investigations into mechanisms of glaucoma induced optic nerve cell death.
Project/Area Number |
10671635
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Ophthalmology
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Research Institution | NIIGATA UNIVERSITY |
Principal Investigator |
ABE Haruki Niigata University, School of Medicine, Department of Ophthalmology, Professor, 医学部, 教授 (40018875)
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Co-Investigator(Kenkyū-buntansha) |
FUKUCHI Takeo Niigata University, University Medical Hospital Assistant, 医学部・附属病院, 助手 (90240770)
SHIRAKASHI Motohiro Niigata University, School of Medicine, Department of Ophthalmology, Lecturer, 医学部・附属病院, 講師 (50242417)
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Project Period (FY) |
1998 – 1999
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Keywords | rat experimental glaucoma model / blockage of axinal transport / degenerative mitochondria / retinal ganglion cell death / caspase 3 / Scanning laser polarimeter / retinal nerve fiber layer |
Research Abstract |
The summary of the clinical study : Using a scanning laser polarimeter, we measured the thickness of retinal nerve fiber layer (RNFLT) in 120 eyes of 60 normal subjects. Measurements were made along the peripapillary ring with the diameter of 1.75 disc diameter and another one 0.8 mm away from the disc margin. The RNFLT was not significantly correlated with age along the two rings. However, the RNFLT ratio of total/nasal area significantly decreased with increase in age. There was an increase in the difference of RNFLT between both eyes with increase in age. In spite of interindivividual variations, the RNFLT along both rings showed age-related changes in subjects. By neurobiological examinations, the experiments using monkey eyes showed that the glaucomatous optic nerve head expressed TGF-β more than that of normal in monkey eyes. This might be related progression of glaucomatous optic disc cupping. The glaucomatous monkey eyes showed lower expression of neurotrophins, NGF, BDNF and CNRF, instead higher expression of Trk B and CNTFR than those in normal eyes. Neurotrophic factors may relate with glaucoma induced optic nerve damage. In addition, degenerative mitochondria with disrupted outer membrane observed in swollen axons and higher expression of caspase 3 in the retinal nerve fiber layer seen in the rat experimental glaucoma model suggested possibility of the release of cytochrome c into cytosol which was known to behave as a critical switch in apoptotic cascade.
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