Early in diabetic retinopathy, long before the appearance of the typical microaneurysms and retinal hemorrhages that have been traditionally used to initiate treatments and diabetic retinopathy, there is now recognized a chronic inflammatory irreversible destruction of all layers of retinal neurons that restricts visual improvement among the trials that are conducted when later ischemia or edema are recognized . In animal studies non- thermal, high-density micropulsed retinal laser treatment has been demonstrated to produce anti-inflammatory and neuro-reparative cytokines that improve retinal pigment epithelium function, as well as retinal vascular autoregulation, while reducing the markers of chronic inflammation, and neurodegeneration). The generated reparative enzymes that have thus far been measured include reductions in thiobarbituric acid reactive substances (TBARS), increased glutathione (GSH) and superoxide dismutase 1 (SOD1) as well as a reduction in cytochrome c, caspase 3 expression and activity along with cleaved caspase 9, and increased Beclin 1, p62, and LC3b). Reductions in markers of inflammation have also been documented in human diabetic retinopathy, and micropulsed laser treatment has been demonstrated to improved early forms of macular edema with significant improvement in vision and without evidence of laser injury. When the macular edema is more severe, however, similar to the studies of intravitreal anti-VEGF injections, the studies of micropulsed laser demonstrate only minimal improvement in the edema and in vision (presumably because of the already established, irreversible neurodegeneration). Studies are underway to investigate the ability of this non-invasive micropulse laser treatment to retard the progressive neuronal apoptosis and vision loss.

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