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Open AccessJournal ArticleDOI

A biomechanical paradigm for axonal insult within the optic nerve head in aging and glaucoma.

Claude F. Burgoyne
- 01 Aug 2011 - 
- Vol. 93, Iss: 2, pp 120-132
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TLDR
A biomechanical framework is provided that the ONH astrocytes and glia fundamentally support and influence both the lamina cribrosa extracellular matrix and retinal ganglion cell axon physiology.
About
This article is published in Experimental Eye Research.The article was published on 2011-08-01 and is currently open access. It has received 350 citations till now. The article focuses on the topics: Optic disk & Optic nerve.

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Citations
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Journal ArticleDOI

The molecular basis of retinal ganglion cell death in glaucoma.

TL;DR: This body of work has considerably updated and expanded the view of how RGCs might die in glaucoma and has revealed novel, potential targets for neuroprotection.
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Optical coherence tomography angiography: A comprehensive review of current methods and clinical applications.

TL;DR: The methods used to create OCTA images, the practical applications of OCTA in light of invasive dye‐imaging studies (e.g. fluorescein angiography) and clinical studies demonstrating the utility of OCT a for research and clinical practice are discussed.
Journal ArticleDOI

Doppler Optical Coherence Tomography

TL;DR: As compared to standard techniques such as fluorescein and indocyanine-green angiography the technique offers two major advantages: no dye is required and depth resolution is required is provided.
Journal ArticleDOI

Under Pressure: Cellular and Molecular Responses During Glaucoma, a Common Neurodegeneration with Axonopathy

TL;DR: This review discusses recent studies that have contributed to understanding the etiology and pathogenesis of glaucoma, and identifies areas that require further investigation and focus on mechanisms identified in other neurodegenerations that may contribute to RGC dysfunction and demise in glAUcoma.
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Critical pathogenic events underlying progression of neurodegeneration in glaucoma.

TL;DR: While ganglion cell somatic drop-out is later in progression, some evidence suggests that synaptic and dendritic pruning in the retina may be a more dynamic process, which offers the possibility that intrinsic self-repair pathways counter pathogenic mechanisms to delay as long as possible outright loss of tissue.
References
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Journal ArticleDOI

The Way Things Move: Looking Under the Hood of Molecular Motor Proteins

TL;DR: The microtubule-based kinesin motors and actin-based myosin motors generate motions associated with intracellular trafficking, cell division, and muscle contraction using a common core structure and convert energy from adenosine triphosphate into protein motion using a similar conformational change strategy.
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The axonal transport of mitochondria

TL;DR: Why mitochondria move and how they move is reviewed, focusing particularly on recent studies of transport regulation, which implicate control of motor activity by specific cell-signaling pathways, regulation of motor access to transport tracks and static microtubule–mitochondrion linkers.
Journal ArticleDOI

Optic nerve damage in human glaucoma. II. The site of injury and susceptibility to damage.

TL;DR: Scanning electron microscopic analysis suggests that the structure of the lamina cribrosa is an important determinant of the degree of susceptibility to damage by elevated intraocular pressure.
Journal ArticleDOI

The optic nerve head as a biomechanical structure: a new paradigm for understanding the role of IOP-related stress and strain in the pathophysiology of glaucomatous optic nerve head damage.

TL;DR: Modeling the ONH as a biomechanical structure generates a group of testable hypotheses regarding the central mechanisms of glaucomatous damage and provides a logic for classifying the principal components of the susceptibility of an individual ONH to a given level of IOP.
Journal Article

Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis.

TL;DR: Some retinal ganglion cells injured by glaucoma and by axotomy die by apoptosis, possibly because of the small proportion of cells that were dying at any given time.
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