Purpose. To quantify the extent and pattern of retinal ganglion cell (RGC) loss in the DBA2/NNia glaucomatous mouse strain as a function of age and compare it with ganglion cell loss in a nonglaucomatous strain. methods. All the ganglion cells in retinas of DBA/2NNia and C57/BL6 mice of various ages (five eyes per age group in 3-month intervals from 3 to 18 months of age) were counted. A novel counting method that does not rely on sampling and that uses retrograde labeling of RGCs with Fluorogold (Fluorochrome; Englewood, CO) was used. RGC loss in the glaucomatous DBA/2NNia mouse strain was contrasted to RGC loss in C57 mice at the same ages. The total number of Fluorogold-labeled cells per retina was compared within and among the two strains as a function of age. In addition, RGC density maps were constructed for each retina, and the range of densities for each age group was compared within and among the two strains. IOP in awake, nonsedated DBA/2NNia mice was measured with a rebound tonometer. results. RGC loss started between 12 and 15 months of age in C57 mice and led to an approximate 46% reduction by 18 months of age. The rate of loss was best approximated by a second-order polynomial curve. In comparison, DBA/2NNia mice also began showing RGC loss at approximately 12 months of age, but it proceeded at a much faster rate, with approximately 64% of their RGCs dying by the 15th month of age but little additional loss thereafter. RGC loss in the DBA animals had a focal pattern that appeared more patchy and showed greater variability than the age-related loss in C57 mice, which was more diffuse. IOP and total retinal area in DBA/2NNia mice began to increase at approximately 6 months of age. IOP normalized after the 12th month of age. conclusions. Age-related RGC loss of up to 50% can occur in the C57 mouse by 18 months of age. The loss does not proceed linearly with age, as is often assumed, and differs both in extent and locational pattern from pathologic RGC loss secondary to glaucoma in DBA/2NNia mouse retinas.

NONARTERITIC anterior ischemic optic neuropathy (NAION) is a disease characterized by sudden, painless, mostly irreversible, and generally nonprogressive visual loss accompanied by nerve fiber bundle field defects, a relative afferent pupillary defect, and optic disc edema. The pathophysiologic characteristics of NAION remains unclear. Although several risk factors have been associated with this relatively common condition, the exact mechanism(s) that lead to optic nerve infarction remain unknown. Risk factors include aging, a small optic nerve head, and microvascular changes associated with diabetes and systemic hypertension.¹ No treatment is available since neither steroids nor surgical optic nerve sheath fenestration has proved to be effective. Prevention with aspirin has not been demonstrated to be effective, although it is recommended.²

Making blind retinas see again: Photoreceptor degeneration is an important cause of blindness. Nelidova et al. used tunable, near-infrared sensors to render diseased photoreceptors light sensitive again (see the Perspective by Franke and Vlasits). Gold nanorods capable of detecting infrared light were coupled with an antibody to temperature-sensitive ion channels. When the nanorods absorbed light and converted it into heat, the coupled ion channels were gated by infrared light. In a mouse model of retinal degeneration, these ion channels were successfully targeted to cone photoreceptors, and responses to near infrared light could be detected. In the primary visual cortex, more cells responded to near-infrared stimuli in mice expressing these ion channels than in controls. By changing the length of the gold nanorods, the system could be tuned to different infrared wavelengths. Science , this issue p. 1108 ; see also p. 1057