scholarly journals Role of Oxidative Stress in Ocular Diseases Associated with Retinal Ganglion Cells Degeneration

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1948
Author(s):  
Eugene Yu-Chuan Kang ◽  
Pei-Kang Liu ◽  
Yao-Tseng Wen ◽  
Peter M. J. Quinn ◽  
Sarah R. Levi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Optic Nerve ◽  
Optic Neuropathy ◽  
Energy Demand ◽  
Neurodegenerative Disorder ◽  
Visual Field Defects ◽  
Ischemic Optic Neuropathy ◽  
Retinal Ganglion ◽  
Ocular Diseases

Ocular diseases associated with retinal ganglion cell (RGC) degeneration is the most common neurodegenerative disorder that causes irreversible blindness worldwide. It is characterized by visual field defects and progressive optic nerve atrophy. The underlying pathophysiology and mechanisms of RGC degeneration in several ocular diseases remain largely unknown. RGCs are a population of central nervous system neurons, with their soma located in the retina and long axons that extend through the optic nerve to form distal terminals and connections in the brain. Because of this unique cytoarchitecture and highly compartmentalized energy demand, RGCs are highly mitochondrial-dependent for adenosine triphosphate (ATP) production. Recently, oxidative stress and mitochondrial dysfunction have been found to be the principal mechanisms in RGC degeneration as well as in other neurodegenerative disorders. Here, we review the role of oxidative stress in several ocular diseases associated with RGC degenerations, including glaucoma, hereditary optic atrophy, inflammatory optic neuritis, ischemic optic neuropathy, traumatic optic neuropathy, and drug toxicity. We also review experimental approaches using cell and animal models for research on the underlying mechanisms of RGC degeneration. Lastly, we discuss the application of antioxidants as a potential future therapy for the ocular diseases associated with RGC degenerations.

scholarly journals Oxidative Stress in Optic Neuropathies

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1538
Author(s):  
Berta Sanz-Morello ◽  
Hamid Ahmadi ◽  
Rupali Vohra ◽  
Sarkis Saruhanian ◽  
Kristine Karla Freude ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Optic Neuropathy ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Redox System ◽  
Ischemic Optic Neuropathy ◽  
Retinal Ganglion ◽  
Oxidative Stress Biomarkers ◽  
Optic Disc Drusen ◽  
Advanced Stages

Increasing evidence indicates that changes in the redox system may contribute to the pathogenesis of multiple optic neuropathies. Optic neuropathies are characterized by the neurodegeneration of the inner-most retinal neurons, the retinal ganglion cells (RGCs), and their axons, which form the optic nerve. Often, optic neuropathies are asymptomatic until advanced stages, when visual impairment or blindness is unavoidable despite existing treatments. In this review, we describe systemic and, whenever possible, ocular redox dysregulations observed in patients with glaucoma, ischemic optic neuropathy, optic neuritis, hereditary optic neuropathies (i.e., Leber’s hereditary optic neuropathy and autosomal dominant optic atrophy), nutritional and toxic optic neuropathies, and optic disc drusen. We discuss aspects related to anti/oxidative stress biomarkers that need further investigation and features related to study design that should be optimized to generate more valuable and comparable results. Understanding the role of oxidative stress in optic neuropathies can serve to develop therapeutic strategies directed at the redox system to arrest the neurodegenerative processes in the retina and RGCs and ultimately prevent vision loss.

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

2017 ◽  
Vol 375 ◽  
pp. 430-441 ◽  
Author(s):  
Saba Khalilpour ◽  
Shahrzad Latifi ◽  
Ghazaleh Behnammanesh ◽  
Amin Malik Shah Abdul Majid ◽  
Aman Shah Abdul Majid ◽  
...  
Keyword(s):  
Optic Neuropathy ◽  
Axonal Degeneration ◽  
Neurodegenerative Disorder ◽  
Pathogenic Mechanism ◽  
Ischemic Optic Neuropathy

scholarly journals Optic Nerve Head Microcirculation in Eyes with Vogt-Koyanagi-Harada Disease Accompanied by Anterior Ischemic Optic Neuropathy

2021 ◽  
pp. 899-908
Author(s):  
Yui Yamashita ◽  
Yuki Hashimoto ◽  
Kenichi Namba ◽  
Kazuomi Mizuuchi ◽  
Susumu Ishida
Keyword(s):  
Optic Nerve ◽  
Visual Field ◽  
Optic Disc ◽  
Optic Neuropathy ◽  
Optic Nerve Head ◽  
Visual Field Defects ◽  
Ischemic Optic Neuropathy ◽  
Optic Disc Swelling ◽  
Vkh Disease ◽  
Field Defects

Anterior ischemic optic neuropathy (AION) is infrequently complicated with Vogt-Koyanagi-Harada (VKH) disease. We quantitatively examined sequential changes in the morphology and circulation hemodynamics, using a C-scan of optical coherence tomography (OCT) and laser speckle flowgraphy (LSFG) in a patient with VKH disease accompanied by AION. A 65-year-old female complained of blurred vision in both of her eyes. The patient presented with optic disc swelling and remarkable choroidal thickening detected by OCT bilaterally. The diagnosis of VKH disease was established based on the presence of pleocytosis detected in the cerebrospinal fluid and hypofluorescent dark dots scattered all around the fundus, detected by indocyanine green angiography. Goldmann perimetry detected visual field defects, similar to superior altitudinal hemianopsia in the right eye and similar to inferior altitudinal hemianopsia in the left eye. The patient was suspected to have developed AION in both eyes. The patient received methylprednisolone pulse therapy, followed by oral prednisolone. With these treatments, the optic disc swelling disappeared. However, optic disc atrophy with visual field defects remained in both eyes. An OCT C-scan showed the ganglion cell complex (GCC) and circumpapillary retinal nerve fiber layer (cpRNFL) thickness getting thinner below the normal range, and LSFG showed the decrease in optic nerve head (ONH) tissue microcirculation. These results supported the occurrence of AION in this patient with VKH disease. The analysis of GCC and cpRNFL thickness and ONH microcirculation would be useful for supporting the occurrence of AION in a case of VKH disease.

Efficacy of Vincamine treatment in a rat model of anterior ischemic optic neuropathy

2020 ◽  
pp. 112067212097428
Author(s):  
Lu Li ◽  
Yu Su ◽  
Juejun Liu ◽  
Changzheng Chen
Keyword(s):  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Optic Neuropathy ◽  
Rat Model ◽  
Ganglion Cells ◽  
Nutrition Therapy ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Retinal Ganglion ◽  
Ischemic Tissue

Non-arteritic anterior ischemic optic neuropathy (NAION) is characterized by the progressive and irreversible death of retinal ganglion cells (RGCs) which is caused by the insufficient blood supply to the optic nerve (ON) head. At present, hormone therapy is used to reduce optic edema, followed by nerve nutrition therapy to protect the ON. However, no surgical or medical therapy has proven to be beneficial consistently in treating NAION. Vincamine is an alkaloid extracted from the Apocynaceae Vinca plant. Vincamine and its derivatives acting as cerebral vasodilators can easily cross the blood-brain barrier, improve the metabolism of ischemic tissue and protect the neuron. In this study, we aimed to investigate the potential neuroprotection of Vincamine in the photodynamic induced rat model of NAION (rAION), to evaluate its effects and possible mechanisms. We found that Vincamine can rescue RGC death and reduce the number of apoptotic cells. The protection of Vincamine might play through the PI3K/Akt/eNOS signaling pathway. Therefore, Vincamine can be an effective therapy method for NAION.

scholarly journals The Difficulty of Diagnosing Invasive Aspergillosis Initially Manifesting as Optic Neuropathy

2019 ◽  
Vol 10 (1) ◽  
pp. 11-18
Author(s):  
Sotaro Mori ◽  
Takuji Kurimoto ◽  
Kana Kawara ◽  
Kaori Ueda ◽  
Mari Sakamoto ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Invasive Aspergillosis ◽  
Optic Neuropathy ◽  
Fungal Infections ◽  
Pulse Therapy ◽  
Visual Field Defects ◽  
Ischemic Optic Neuropathy ◽  
Light Perception ◽  
Steroid Pulse ◽  
The Right

Background: Invasive aspergillosis is often fatal. Here, we report a patient with invasive aspergillosis primarily involving the optic nerve diagnosed on autopsy. Case Presentation: A 77-year-old female with underlying diabetes mellitus, hyperlipidemia, and hypertension presented with disc swelling of the left eye. Although mini-pulse steroid therapy improved visual acuity (VA) of the left eye, it abruptly decreased to no light perception within a month, followed by a decrease in VA of the right eye to 0.5. At referral, VA was 0.3 in the right eye, and there was no light perception in the left eye. Results: Fundus examination revealed optic disc swelling of both eyes. Goldmann perimetry showed irregular visual field defects, whereas magnetic resonance imaging (MRI), general, and cerebrospinal fluid (CSF) examinations revealed no distinct abnormalities. We suspected anterior ischemic optic neuropathy and invasive optic neuropathy. As with the left eye, steroid pulse therapy temporarily improved VA of the right eye and then decreased to 0.2. Additional anticoagulant therapy did not improve VA. Concurrent to therapy, the patient became febrile with depressed consciousness. Repeat MRI identified suspected midbrain infarction, and CSF examination indicated cerebral meningitis. In spite of administering transfusions and antibiotics, she died on hospital day 40. Autopsy revealed large amounts of Aspergillus hyphae mainly localized in the dura mater of the optic nerve and destruction of the cerebral artery wall, suggesting an etiology of subarachnoid hemorrhage. Conclusions: When examining refractory and persistent disc swelling, we should rule out fungal infections of the optic nerve.

scholarly journals Optic Nerve Head Microcirculation in Eyes With Vogt-Koyanagi-Harada Disease Accompanied by Anterior Ischemic Optic Neuropathy: a Case Report

2021 ◽  
Author(s):  
Yui Yamashita ◽  
Yuki Hashimoto ◽  
Kenichi Namba ◽  
Kazuomi Mizuuchi ◽  
Susumu Ishida
Keyword(s):  
Optic Nerve ◽  
Visual Field ◽  
Optic Disc ◽  
Optic Neuropathy ◽  
Optic Nerve Head ◽  
Visual Field Defects ◽  
Ischemic Optic Neuropathy ◽  
Optic Disc Swelling ◽  
Vkh Disease ◽  
Field Defects

Abstract Purpose: It has been reported that anterior ischemic optic neuropathy (AION) is an infrequent complication of Vogt-Koyanagi-Harada (VKH) disease; however, the physiological changes have not been understood. We quantitatively examined sequential changes in the morphology and circulation hemodynamics using an optical coherence tomography (OCT) C-scan and laser speckle flowgraphy (LSFG) in a patient with VKH disease accompanied by AION.Case presentation: A 65-year-old female complained of blurred vision in both of her eyes. She presented with optic disc swelling and remarkable choroidal thickening detected by OCT bilaterally. Indocyanine green angiography in the middle phase showed multiple hypofluorescent dark dots scattering around the fundus. With the use of Goldmann perimetry, bilateral visual field defects were detected; these were similar to those of inferior altitudinal hemianopsia. Pleocytosis was detected. The patient was diagnosed with VKH disease, suspected to be accompanied by AION in both eyes. She received methylprednisolone pulse therapy followed by oral prednisolone. With these treatments, optic disc swelling disappeared; however, optic disc atrophy with visual field defects remained in both eyes. An OCT C-scan showed the ganglion cell complex (GCC) and circumpapillary retinal nerve fiber layer (cpRNFL) thickness getting thinner below the normal range, and LSFG showed a decrease in optic nerve head tissue microcirculation during follow-up. These results supported the occurrence of AION in this patient with VKH disease.Conclusion: The analyses of GCC and cpRNFL thicknesses with an OCT C-scan and optic nerve head microcirculation with LSFG would be useful for supporting the occurrence of AION in cases of VKH disease.

scholarly journals Protective Effects of Oroxylin A on Retinal Ganglion Cells in Experimental Model of Anterior Ischemic Optic Neuropathy

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 902
Author(s):  
Jia-Ying Chien ◽  
Shu-Fang Lin ◽  
Yu-Yau Chou ◽  
Chi-Ying F. Huang ◽  
Shun-Ping Huang
Keyword(s):  
Retinal Ganglion Cells ◽  
Optic Neuropathy ◽  
Ganglion Cells ◽  
Ischemic Injury ◽  
Anterior Ischemic Optic Neuropathy ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Ischemic Optic Neuropathy ◽  
Retinal Ganglion ◽  
Oroxylin A

Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common cause of acute vision loss in older people, and there is no effective therapy. The effect of the systemic or local application of steroids for NAION patients remains controversial. Oroxylin A (OA) (5,7-dihydroxy-6-methoxyflavone) is a bioactive flavonoid extracted from Scutellariae baicalensis Georgi. with various beneficial effects, including anti-inflammatory and neuroprotective effects. A previous study showed that OA promotes retinal ganglion cell (RGC) survival after optic nerve (ON) crush injury. The purpose of this research was to further explore the potential actions of OA in ischemic injury in an experimental anterior ischemic optic neuropathy (rAION) rat model induced by photothrombosis. Our results show that OA efficiently attenuated ischemic injury in rats by reducing optic disc edema, the apoptotic death of retinal ganglion cells, and the infiltration of inflammatory cells. Moreover, OA significantly ameliorated the pathologic changes of demyelination, modulated microglial polarization, and preserved visual function after rAION induction. OA activated nuclear factor E2 related factor (Nrf2) signaling and its downstream antioxidant enzymes NAD(P)H:quinone oxidoreductase (NQO-1) and heme oxygenase 1 (HO-1) in the retina. We demonstrated that OA activates Nrf2 signaling, protecting retinal ganglion cells from ischemic injury, in the rAION model and could potentially be used as a therapeutic approach in ischemic optic neuropathy.

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