Abstract
Diabetic retinopathy (DR) is one of the most common retinal diseases world-wide. It has a complex pathology that involves the vasculature of the inner retina and breakdown of the blood-retinal barrier. Extensive research has determined that DR is not only a vascular disease but also has a neurodegenerative component and that essentially all types of cells in the retina are affected, leading to chronic loss of visual function. A great deal of work using animal models of DR has established the loss of neurons and pathology of other cell types, including supporting glial cells. There has also been an increased emphasis on measuring retinal function in the models, as well as further validation and extension of the animal studies by clinical and translational research. This article will attempt to summarize the more recent developments in research towards understanding the complexities of retinal neurodegeneration and functional vision loss in DR.
Highlights
Over the last 20 years the concept that neurodegeneration plays a part in diabetic retinopathy (DR) has become widely accepted
This was a simplistic approach towards a complex disease, and more recent evidence suggests that other processes may contribute to reduced neuronal function and vision loss before cell death occurs; alongside changes in the regulatory mechanisms of the retinal vasculature
These data suggested that while diabetes increased the rate of cell death in the retina, it was the result of a chronic degenerative process that began within weeks after the onset of hyperglycemia
Summary
Immunohistochemical work on retinas from diabetic animal models extended the concept that many of the cells undergoing apoptosis were subtypes of neurons, including retinal ganglion cells and amacrine cells. A follow up study by the same investigators reported even greater loss of tissue thickness in the pericentral ganglion cell layer (5.1 μm) and a loss in the peripheral macula nerve fiber layer (3.7 μm) of patients with Type I diabetes and minimal vascular retinopathy [29]. Reductions in the thickness of the nerve fiber layer are most likely to indicate a reduced abundance of retinal ganglion cell axons, and presumably a loss of the cell bodies and dendrites This deficit is likely to limit the ability to transmit visual information to the brain and compromise the information processing capacity of the inner retina. In most studies the nerve fiber layer loss was apparent in a population of patients that did not have macular edema, suggesting that significant neural degeneration occurred before a clinically apparent loss of vascular barrier function
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