NEURODEGENERATION IN GLAUCOMA: PROGRESSION AND CALCIUM-DEPENDENT INTRACELLULAR MECHANISMS

被引:110
作者
Crish, S. D. [3 ,4 ]
Calkins, D. J. [1 ,2 ]
机构
[1] Vanderbilt Univ, Med Ctr, Vanderbilt Eye Inst, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Med Ctr, Vanderbilt Brain Inst, Nashville, TN 37232 USA
[3] Northeastern Ohio Univ Coll Med & Pharm, Coll Med, Dept Pharmaceut Sci, Rootstown, OH 44272 USA
[4] Northeastern Ohio Univ Coll Med & Pharm, Coll Pharm, Dept Pharmaceut Sci, Rootstown, OH 44272 USA
关键词
axonopathy; axon degeneration; retinal ganglion cell; axonal transport; neurodegeneration; intracellular calcium; OPTIC-NERVE HEAD; RETINAL GANGLION-CELLS; OXIDATIVE STRESS MARKERS; DBA/2J MOUSE MODEL; ELEVATED INTRAOCULAR-PRESSURE; NECROSIS-FACTOR-ALPHA; OPEN-ANGLE GLAUCOMA; OCULAR HYPERTENSION; AXONAL-TRANSPORT; RAT MODEL;
D O I
10.1016/j.neuroscience.2010.12.036
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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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页码:1 / 11
页数:11
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