4.5 Article

NEURODEGENERATION IN GLAUCOMA: PROGRESSION AND CALCIUM-DEPENDENT INTRACELLULAR MECHANISMS

Journal

NEUROSCIENCE
Volume 176, Issue -, Pages 1-11

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2010.12.036

Keywords

axonopathy; axon degeneration; retinal ganglion cell; axonal transport; neurodegeneration; intracellular calcium

Categories

Funding

  1. NIH [EY017427]
  2. Melza M. and Frank Theodore Barr Foundation through the Glaucoma Research Foundation
  3. Research to Prevent Blindness, Inc.
  4. American Health Assistance Foundation
  5. Fight for Sight
  6. Vanderbilt Discovery Science Program
  7. Vanderbilt Vision Research Center [P30EY008126]

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Glaucoma is an age-related optic neuropathy involving sensitivity to ocular pressure. The disease is now seen increasingly as one of the central nervous system, as powerful new approaches highlight an increasing number of similarities with other age-related neurodegenerations such as Alzheimer's and Parkinson's. While the etiologies of these diseases are diverse, they involve many important common elements including compartmentalized programs of degeneration targeting axons, dendrites and finally cell bodies. Most age-related degenerations display early functional deficits that precede actual loss of neuronal substrate. These are linked to several specific neurochemical cascades that can be linked back to dysregulation of Ca2+-dependent processes. We are now in the midst of identifying similar cascades in glaucoma. Here we review recent evidence on the pathological progression of neurodegeneration in glaucoma and some of the Ca2+-dependent mechanisms that could underlie these changes. These mechanisms present clear implications for efforts to develop interventions targeting neuronal loss directly and make glaucoma an attractive model for both interrogating and informing other neurodegenerative diseases. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

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