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This dissertation, "Neuroprotection of Low Energy Laser on Retinal Ganglion Cells Survival After Optic Nerve Injury" by 林瑋源, Wai-yuan, Leon, Lam, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. DOI: 10.5353/th_b3122286 Subjects: Retinal ganglion cells Optic nerve - Wounds and injuries Optic nerve - Laser surgery
Many retinal and optic nerve disorders have no effective therapy, or are treated incompletely and with considerable side effects. Recent advances have suggested the significant benefits associated with neuroprotection - that is, when treatment strategies are directed to photoreceptors, retinal ganglion cells, or other neural targets. Enter Ocular N
We have demonstrated in previous studies that low energy laser reduces injury-induced deficits caused by acute partial injury of the rat optic nerve. The results of in-depth analysis suggest that the laser effect in this model is of a neuroprotective nature. We have devoted the time lapsed since approval of funding of the present study to characterization of the optic nerve partial lesion model, in an attempt to determine whether the progressive degeneration which occurs subsequently to the primary insult and continues in the absence of any external insult, is of a self-perpetuating nature, and whether such progressive degeneration follows any topographical pattern and whether any such pattern might be a reflection of the severity of the primary injury itself. By clarify the above points, we may turn our model into an ideal model for studying the neuroprotection of the optic nerve and retinal ganglion cells from injurious conditions.
This dissertation, "Neuroprotective Effect of Ginkgo Biloba Extract on Retinal Ganglion Cells in a Rat Glaucoma Model" by Ching, Lai, 賴晴, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled Neuroprotective effect of Ginkgo biloba extract on retinal ganglion cells in a rat glaucoma model submitted by Ching Lai for the degree of Master of Philosophy at the University of Hong Kong in August 2003 Glaucoma is a progressive optic neuropathy that ultimately causes retinal ganglion cell (RGC) death and loss of vision. Current therapies on this disease only aim at controlling intraocular pressure (IOP). However, patients undergoing such therapies may still develop RGCs degeneration. Therefore a new "therapy" has been suggested and is named neuroprotection. Neuroprotection aims at protecting and rescuing RGCs from damage. One suggested neuroprotectant is the Ginkgo biloba extract (GBE). GBE is a traditional Chinese medicine, which has been shown to increase ocular blood flow velocity and thus may improve vision. However, the direct effect of GBE on RGCs survival has not been investigated. Therefore, the objective of this study is to investigate the neuroprotective effect of GBE on RGCs in an ocular hypertension model. By using a laser-induced ocular hypertension model, we have demonstrated the neuroprotective effect of GBE on RGC survival. After administered Sprague- Dawley rats with 12 mg/ml, 120 mg/ml and 200 mg/ml GBE, RGC death observed in experimental glaucoma was virtually abolished. The possible neuroprotective mechanisms of GBE on experimental glaucoma were also examined in this study. It has been proposed that GBE protects neurons by modulating glial responses. We found that the number of OX42 immunopositive microglia was increased after GBE treatment in glaucomatous retinas. Based on the morphological analysis, the numbers of both the resting and activated forms of microglia were increased with GBE administration. The protective effect of GBE on RGCs was partially removed by inhibiting the response of microglia with the microglia inhibitory factor. We have also studied the role of other glial cells in protecting RGCs. Macroglia such as astrocytes and Muller cells were studied by quantifying the GFAP immunolabeled glial cells in the glaucomatous retina. Immunoreactivity of GFAP was enhanced after 1.2 mg/ml, 12 mg/ml and 120 mg/ml GBE treatments. In experiments on different survival periods after GBE administration, GBE was shown to induce an earlier onset and a sustained expression of GFAP in the glaucomatous retina when compared with the controls. Application of GBE may therefore be a potentially useful treatment in preventing the loss of vision in glaucoma patients. DOI: 10.5353/th_b2949405 Subjects: Retinal ganglion cells Ginkgo - Therapeutic use Glaucoma Rats as laboratory animals
This book provides the latest findings on neuroprotection and neuroregeneration as potential therapeutic strategies for various eye diseases, namely, glaucoma, age-related macular degeneration (AMD), retinal detachment, and retinitis pigmentosa. Glaucoma is one of the main causes of blindness throughout the world, and other diseases such as AMD and retinitis pigmentosa also lead to loss of vision. All these conditions are characterized by degeneration of specific retinal cell types, making it essential to establish treatments to protect retinal neurons and the optic nerve. With that aim in mind, this book explains the mechanisms underlying aforementioned diseases and their experimental models. The novel strategy proposals for the treatment of retinal diseases based on the concept of neuroprotection are also discussed in the main body of the text, while the section on regenerative research discusses optic nerve regeneration, endothelial progenitor cells, and iPS cells. This book is recommended as a professional reference work for all doctors and trainees in the field of ophthalmology who are interested in neuroprotective and neuroregenerative treatments.
Glaucoma is one of the main causes of blindness throughout the world. It is characterized by death of the retinal ganglion cells, which is associated with loss of the axons making up the optic nerve. Recent studies have demonstrated support for the classification of glaucoma as a degenerative disease of the central nervous system (CNS), leading researchers to look at identifying neuroprotection strategies for the treatment of this disease, like those used for other degenerative diseases of the CNS. This book will provide an in-depth examination of the most recent findings regarding glaucoma, including risk factors, diagnosis, clinical monitoring, treatment, and above all, the need for treatment based on the concept of neuroprotection. A large part of the book is devoted to research related to this new approach to the treatment of glaucoma. Describes the most recent developments on neuroprotection of the optic nerve, including experimental models now used and clinical protocols Discusses new strategies for the prevention of neuronal injury in glaucoma patients Focuses on evidence-based risk factors, innovative diagnostic aspects and advanced medical/surgical treatment of glaucoma
Many retinal and optic nerve disorders have no effective therapy, or are treated incompletely and with considerable side effects. Recent advances have suggested the significant benefits associated with neuroprotection - that is, when treatment strategies are directed to photoreceptors, retinal ganglion cells, or other neural targets. Enter Ocular Neuroprotection, the only handbook of research methods in neuroprotection of ocular disease covering both laboratory and clinical levels, to aid researchers studying the prevention of neuronal death from these and other hard-to-treat ophthalmic disorders.