![]() ![]() 6, 7 Abnormalities of cytoskeletal proteins such as neurofilament (NF) have also been demonstrated in experimental models of glaucoma 8– 10 and may represent a mechanism of susceptibility. For example, in experimental models of RGC injury such as optic nerve transection (ONT) or crush, there is a delay among the majority of surviving RGCs before axonal caliber begins to decline, 5 which is preceded by changes in cytoskeletal protein content and mRNA. 4 This has clinical relevance because cytoskeletal abnormalities might develop in diseases such as glaucoma prior to RGC death. 1– 3 This is supported both by theoretical analyses 1, 2 and by evidence demonstrating that RNFL birefringence rapidly declines after chemical disruption of cytoskeletal components, microtubules (MT) in particular, in situ 3 or in vivo. Previous studies have shown that cytoskeletal components and their tertiary structure within retinal ganglion cell (RGC) axons cause the retinal nerve fiber layer (RNFL) to exhibit the optical property of form birefringence.
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