Ischemic optic neuropathy as a model of neurodegenerative disorder: A review of pathogenic mechanism of axonal degeneration and the role of neuroprotection

Abstract Optic neuropathy is a neurodegenerative disease which involves optic nerve injury. It is caused by acute or intermittent insults leading to visual dysfunction. Deterioration and loss of visual function characterize optic neuropathy. There are number of factors, responsible for optic neuropa...

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Bibliographic Details
Published in:Journal of the neurological sciences 2017-04, Vol.375, p.430-441
Main Authors: Khalilpour, Saba, Latifi, Shahrzad, Behnammanesh, Ghazaleh, Majid, Amin Malik Shah Abdul, Majid, Aman Shah Abdul, Tamayol, Ali
Format: Article
Language:English
Subjects:
Angiogenesis
Animals
Apoptosis - drug effects
Axons - pathology
Disease Models, Animal
Excitotoxicity
Humans
Ischemic optic neuropathy
Neurodegenerative Diseases - etiology
Neurodegenerative Diseases - prevention & control
Neuroinflammation
Neurology
Neuroprotection
Neuroprotection - physiology
Optic Neuropathy, Ischemic - complications
Oxidative stress
Oxidative Stress - physiology
Retinal Ganglion Cells - pathology
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Summary:Abstract Optic neuropathy is a neurodegenerative disease which involves optic nerve injury. It is caused by acute or intermittent insults leading to visual dysfunction. Deterioration and loss of visual function characterize optic neuropathy. There are number of factors, responsible for optic neuropathy, and the optic nerve axon is affected in all type which causes the loss of retinal ganglion cells. In this review we will highlight the pathogenic mechanisms associated with the cell loss cascades occurred during axonal degeneration and ischemic optic neuropathy. Mechanisms such as oxidative stress, excitotoxicity, angiogenesis, neuroinflammation and apoptosis following retinal ischemia, will be investigated. We will also discuss the effect of neuroprotective agents in attenuation of the negative effect of factors involve in the disease occurrence and progression.
ISSN:0022-510X
1878-5883
DOI:10.1016/j.jns.2016.12.044