Article

Optic Nerve Disease and Axon Pathophysiology

Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
International Review of Neurobiology (Impact Factor: 1.92). 12/2012; 105:1-17. DOI: 10.1016/B978-0-12-398309-1.00002-0
Source: PubMed

ABSTRACT

Optic neuropathy is the most common cause of irreversible blindness worldwide. Although the most common optic neuropathy is glaucoma, there are also many other optic neuropathies, for example, those associated with multiple sclerosis, giant cell arteritis, ischemia, and many other diseases. In almost all cases, the pathogenesis involves injury to the retinal ganglion cell axon, with consequent somal and axonal degeneration. This chapter reviews the clinical and pathophysiological properties associated with three of the most common optic neuropathies, as well as recent findings in understanding axonal degeneration. It concludes with a status report on therapies for optic nerve disease, including axoprotection, an approach being studied that has the goal of maintaining axonal integrity and function after injury.

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Available from: Alireza Ghaffarieh, Dec 13, 2014
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    • "In contrast to the progressive nature of glaucoma, acute optic neuropathies are characterized by the acute onset of visual loss and are usually caused by ischemia (ischemic optic neuropathies), traumatic brain injury (traumatic optic neuropathy), and infection or inflammation (optic neuritis). Other causes of optic nerve injury, with varied clinical presentations , are compression, toxic or nutritional causes, infiltration of neoplastic or inflammatory cells, and papilledema secondary to elevated intracranial pressure [1] [6] [7]. Optic neuropathy can also occur in hereditary neurodegenerative disorders related to primary mitochondrial dysfunction, as well as in two nonsyndromic mitochondrial hereditary optic neuropathies: Leber hereditary optic neuropathy and experience has accumulated in the transplantation of BM- MSCs and BM-MNCs in patients with neurological disorders, indicating the safety and the feasibility of this approach [36]. "
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    ABSTRACT: Cell cycle re-entry is one of the key processes in neuronal apoptosis. Previous studies have shown that Ski-interacting protein (SKIP) played an important role in cell cycle re-entry. However, its expression and function in optic nerve injury are still with limited acquaintance. To investigate whether SKIP is involved in retinal ganglion cells (RGCs) death, we performed an optic nerve crush (ONC) model in adult rats. Western blot analysis revealed that up-regulation of SKIP was present in retina at 5 days after ONC. Immunofluorescent labeling indicated that up-regulated SKIP was found mainly in RGCs. We also investigated co-localization of SKIP with active-caspase-3 and TUNEL (apoptotic markers) -positive cells in the retina after ONC. In addition, the expression of SKIP was increased in parallel with P53 and P21 in retina after ONC. All these results suggested that up-regulation of SKIP in the retina was associated with RGCs death after ONC.
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