Visual Neuroscience



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


RICHARD T.  LIBBY  a1 , MICHAEL G.  ANDERSON  a1 a2 p1 , IOK-HOU  PANG  a3 , ZACHARY H.  ROBINSON  a1 a2 , OLGA V.  SAVINOVA  a1 a2 , I. MIHAI  COSMA  a1 , AMY  SNOW  a1 a2 , LAWRISTON A.  WILSON  a1 a2 , RICHARD S.  SMITH  a1 a2 , ABBOT F.  CLARK  a3 and SIMON W.M.  JOHN  a1 a2 a4 c1
a1 The Jackson Laboratory, Bar Harbor
a2 The Howard Hughes Medical Institute, Bar Harbor
a3 Alcon Research, Ltd. Ft. Worth
a4 Department of Ophthalmology, Tufts University School of Medicine, Boston

Article author query
libby rt   [Google Scholar] 
anderson mg   [Google Scholar] 
pang i   [Google Scholar] 
robinson zh   [Google Scholar] 
savinova ov   [Google Scholar] 
cosma im   [Google Scholar] 
snow a   [Google Scholar] 
wilson la   [Google Scholar] 
smith rs   [Google Scholar] 
clark af   [Google Scholar] 
john swm   [Google Scholar] 
 

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.

(Received March 8 2005)
(Accepted May 19 2005)


Key Words: Glaucoma; Mouse model; Intraocular pressure; Neurodegeneration.

Correspondence:
c1 Address correspondence and reprint requests to: Simon W.M. John, The Howard Hughes Medical Institute, The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA. E-mail: swmj@jax.org
p1 Current address of Michael G. Anderson: Department of Physiology and Biophysics. The University of Iowa, Iowa City, IA, 52242, USA