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

Published online by Cambridge University Press:  06 December 2005

RICHARD T. LIBBY
Affiliation:
The Jackson Laboratory, Bar Harbor
MICHAEL G. ANDERSON
Affiliation:
The Jackson Laboratory, Bar Harbor The Howard Hughes Medical Institute, Bar Harbor Current address of Michael G. Anderson: Department of Physiology and Biophysics. The University of Iowa, Iowa City, IA, 52242, USA
IOK-HOU PANG
Affiliation:
Alcon Research, Ltd. Ft. Worth
ZACHARY H. ROBINSON
Affiliation:
The Jackson Laboratory, Bar Harbor The Howard Hughes Medical Institute, Bar Harbor
OLGA V. SAVINOVA
Affiliation:
The Jackson Laboratory, Bar Harbor The Howard Hughes Medical Institute, Bar Harbor
I. MIHAI COSMA
Affiliation:
The Jackson Laboratory, Bar Harbor
AMY SNOW
Affiliation:
The Jackson Laboratory, Bar Harbor The Howard Hughes Medical Institute, Bar Harbor
LAWRISTON A. WILSON
Affiliation:
The Jackson Laboratory, Bar Harbor The Howard Hughes Medical Institute, Bar Harbor
RICHARD S. SMITH
Affiliation:
The Jackson Laboratory, Bar Harbor The Howard Hughes Medical Institute, Bar Harbor
ABBOT F. CLARK
Affiliation:
Alcon Research, Ltd. Ft. Worth
SIMON W.M. JOHN
Affiliation:
The Jackson Laboratory, Bar Harbor The Howard Hughes Medical Institute, Bar Harbor Department of Ophthalmology, Tufts University School of Medicine, Boston

Abstract

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.

Type
Research Article
Copyright
© 2005 Cambridge University Press

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