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Abstract #25666 Published in IGR 12-2
Distal axonopathy with structural persistence in glaucomatous neurodegeneration
Crish SD; Sappington RM; Inman DM; Horner PJ; Calkins DJProceedings of the National Academy of Sciences of the United States of America 2010; 107: 5196-5201
See also comment(s) by Leonard A. Levin •
An early hallmark of neuronal degeneration is distal transport loss and axon pathology. Glaucoma involves the degeneration of retinal ganglion cell (RGC) neurons and their axons in the optic nerve. Here we show that, like other neurodegenerations, distal axon injury appears early inmouse glaucoma.Where RGC axons terminate in the superior colliculus, reduction of active transport follows a retinotopic patternresemblingglaucomatous visionloss. Like glaucoma, susceptibility to transport deficits increases with age and is not necessarily associatedwith elevated ocular pressure. Transport deficits progress distal-to-proximal, appearing in the colliculus first followed by more proximal secondary targets and then the optic tract. Transport persists through the optic nerve head before finally failing in the retina. Although axon degeneration also progresses distal-to-proximal, myelinated RGC axons and their presynaptic terminals persist in the colliculus well after transport fails. Thus, distal transport loss is predegenerative and may represent a therapeutic target.
D. J. Calkins. Vanderbilt Eye Institute, Vanderbilt Brain Institute, Vanderbilt University Medical Center, Nashville, TN 37232, United States. david.j.calkins@vanderbilt.edu
Classification:
2.13 Retina and retinal nerve fibre layer (Part of: 2 Anatomical structures in glaucoma)
11.8 Neuroprotection (Part of: 11 Medical treatment)
3.9 Pathophysiology (Part of: 3 Laboratory methods)
