Inherited glaucoma in DBA/2J mice: Pertinent disease features for studying the neurodegeneration

The glaucomas are neurodegenerative diseases involving death of retinal ganglion cells and optic nerve head excavation. A major risk factor for this neurodegeneration is a harmfully elevated intraocular pressure (IOP). Human glaucomas are typically complex, progressive diseases that are prevalent in...

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Published inVisual neuroscience Vol. 22; no. 5; pp. 637 - 648
Main Authors LIBBY, RICHARD T., ANDERSON, MICHAEL G., PANG, IOK-HOU, ROBINSON, ZACHARY H., SAVINOVA, OLGA V., COSMA, I. MIHAI, SNOW, AMY, WILSON, LAWRISTON A., SMITH, RICHARD S., CLARK, ABBOT F., JOHN, SIMON W.M.
Format Journal Article
LanguageEnglish
Published New York, USA Cambridge University Press 01.09.2005
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Summary:The glaucomas are neurodegenerative diseases involving death of retinal ganglion cells and optic nerve head excavation. A major risk factor for this neurodegeneration is a harmfully elevated intraocular pressure (IOP). Human glaucomas are typically complex, progressive diseases that are prevalent in the elderly. Family history and genetic factors are clearly important in human glaucoma. Mouse studies have proven helpful for investigating the genetic and mechanistic basis of complex diseases. We previously reported inherited, age-related progressive glaucoma in DBA/2J mice. Here, we report our updated findings from studying the disease in a large number of DBA/2J mice. The period when mice have elevated IOP extends from 6 months to 16 months, with 8–9 months representing an important transition to high IOP for many mice. Optic nerve degeneration follows IOP elevation, with the majority of optic nerves being severely damaged by 12 months of age. This information should help with the design of experiments, and we present the data in a manner that will be useful for future studies of retinal ganglion cell degeneration and optic neuropathy.
Bibliography:ark:/67375/6GQ-VJVNBV0M-B
PII:S0952523805225130
istex:855EFDED33F9C6D56CF467FAA0428215EBC9BD49
PMID:16332275
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0952-5238
1469-8714
DOI:10.1017/S0952523805225130