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Editors Selection IGR 11-3
Progression: Reversibility of progression
Comment by Leonard A. Levin on:
25666 Distal axonopathy with structural persistence in glaucomatous neurodegeneration, Crish SD; Sappington RM; Inman DM et al., Proceedings of the National Academy of Sciences of the United States of America, 2010; 107: 5196-5201
The paper by Crish et al. (581) is significant because it shows that distal loss of axonal transport early the course of disease in two different mouse models of glaucoma. The DBA/2 mouse, which undergoes pigmentary dispersion, inflammation, and secondary angle closure, and injection of microbeads to block trabecular outflow, both showed decrease transport of cholera toxin β-subunit to distal terminals of retinal ganglion cell (RGC) axons in the superior colliculus, followed over time by more proximal loss of transport. This occurred even though the axons themselves maintained structural integrity.
The loss of visual function early in the course of disease may be more reversible than previously believed
Given that at least two different groups (Howell et al. J Cell Biol 2007; 179: 1523-1537; Soto et al. J Neurosci 2008; 28: 548-561) have shown that the site of initial axon integrity loss (and presumably injury) in the DBA/2 mouse occurs at the optic nerve head, and that several studies have provided direct and indirect evidence that the site of primary injury in glaucoma occurs at or around the optic nerve head, these results indicate that the effects of the proximal RGC injury can initially be detected at its most distal termination in glaucoma (and potentially other optic neuropathies, although that was not studied). Not only do these findings lend support to studies showing that lateral geniculate changes may be an early finding in glaucoma (reviewed in Yücel Y, Gupta N. Prog Brain Res 2008; 173: 465-478) but they also suggest that the loss of visual function early in the course of disease may be more reversible than previously believed.
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