have increased apoptosis of retinal ganglion cells and other cells of the neural retina. Glial cells showed evidence of concurrent degeneration, proliferation, and activation (99).

Therapies or Gene Modifications Studied in this Model

The list of therapies or genes studied with respect to their role in the pathogenesis of diabetic retinopathy in mice is rapidly growing (see Table 3). This model continues to provide new insight into the pathogenesis of retinopathy, especially via genetic manipulation.

Advantages and Disadvantages of the Model

Advantages of mice are that genetic modifications are becoming relatively easy to achieve, reagents and antibodies are readily available, housing is inexpensive, and the histopathology develops relatively quickly (at a rate similar to that in diabetic rats). A concern about the model mainly is related to the very early (and modest) histopathology that has been found to develop within the lifespan of diabetic animals. Whether or not C57Bl/6J mice are protected from diabetes-induced neurodegeneration also needs to be resolved.

OTHER RODENTS

Diabetic hamsters have been reported to develop the usual spectrum of lesions, including acellular capillaries, pericyte loss, and endothelial proliferation, but they have not been found to develop microaneurysms or neovascularization (108).

NONDIABETIC MODELS THAT DEVELOP ASPECTS

OF DIABETIC-LIKE RETINOPATHY

Galactose Feeding

Nondiabetic dogs fed a diet enriched with 30% galactose developed a retinopathy that was indistinguishable from that of diabetic dogs and patients, including microaneurysms, vaso-obliteration, pericyte ghosts, and hemorrhages (12, 30, 109–119). Likewise,

Table 3

Therapies or Genes Studied in Mouse Diabetic Retinopathy Models