Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 107, Issue 11, Pages 5196-5201Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0913141107
Keywords
axon transport; optic neuropathy; retinal ganglion cell; glaucoma; optic nerve
Categories
Funding
- Glaucoma Research Foundation
- Unrestricted Departmental
- American Health Assistance Foundation
- Vanderbilt Discovery
- National Institutes of Health [EY017427]
- Vanderbilt Vision Research Center Core [5P30EY008126-19]
- Fight for Sight
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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 pattern resembling glaucomatous vision loss. Like glaucoma, susceptibility to transport deficits increases with age and is not necessarily associated with 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.
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