Essential iris atrophy, pigment dispersion, and glaucoma in DBA/2J mice.

TLDR

The DBA/2J mouse strain is a valuable model for studying pressure‑related ganglion cell death, optic nerve atrophy, and neuroprotective strategies. This study aimed to characterize ocular abnormalities linked to iris atrophy in DBA/2J mice and assess whether they develop elevated intraocular pressure and glaucoma. Researchers examined eyes from 2‑ to 30‑month‑old mice using slit‑lamp biomicroscopy, ophthalmoscopy, ultrasound backscatter microscopy, histology, and IOP measurements. DBA/2J mice exhibit progressive pigment dispersion, iris atrophy, synechias, and elevated IOP that, by 9–22 months, lead to retinal ganglion cell loss, optic nerve atrophy, cupping, and a secondary angle‑closure glaucoma phenotype whose severity increases with age.

Abstract

To characterize ocular abnormalities associated with iris atrophy in DBA/2J mice and to determine whether mice of this strain develop elevated intraocular pressure (IOP) and glaucoma.Different approaches, including slit-lamp biomicroscopy, ophthalmoscopic examination, ultrasound backscatter microscopy, and histology were used to examine the eyes of DBA/2J mice ranging from 2 to 30 months old. IOP was measured in DBA/2J mice of different ages.DBA/2J mice were found to develop pigment dispersion, iris transillumination, iris atrophy, anterior synechias, and elevated IOP. IOP was elevated in most mice by the age of 9 months. These changes were followed by the death of retinal ganglion cells, optic nerve atrophy, and optic nerve cupping. The prevalence and severity of these lesions increased with age. Optic nerve atrophy and optic nerve cupping was present in the majority of mice by the age of 22 months.DBA/2J mice develop a progressive form of secondary angle-closure glaucoma that appears to be initiated by iris atrophy and the associated formation of synechias. This mouse strain represents a useful model to evaluate mechanisms of pressure-related ganglion cell death and optic nerve atrophy, and to evaluate strategies for neuroprotection.