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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact.
Book Synopsis Neurodegeneration and Neuroprotection in Retinal Disease by : Giovanni Casini
Download or read book Neurodegeneration and Neuroprotection in Retinal Disease written by Giovanni Casini and published by Frontiers Media SA. This book was released on 2020-08-21 with total page 159 pages. Available in PDF, EPUB and Kindle. Book excerpt: This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact.
Book Synopsis Neurodegeneration and Neuroprotection in Retinal Disease, Volume II by : Giovanni Casini
Download or read book Neurodegeneration and Neuroprotection in Retinal Disease, Volume II written by Giovanni Casini and published by Frontiers Media SA. This book was released on 2022-10-03 with total page 127 pages. Available in PDF, EPUB and Kindle. Book excerpt:
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.
Book Synopsis Neuroprotection and Neuroregeneration for Retinal Diseases by : Toru Nakazawa
Download or read book Neuroprotection and Neuroregeneration for Retinal Diseases written by Toru Nakazawa and published by Springer. This book was released on 2014-07-23 with total page 351 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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.
This book addresses approaches to the treatment of retinal diseases, targeting common processes and components.
Book Synopsis Therapies for Retinal Degeneration by : de la Rosa (Enrique J.)
Download or read book Therapies for Retinal Degeneration written by de la Rosa (Enrique J.) and published by Royal Society of Chemistry. This book was released on 2018 with total page 276 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book addresses approaches to the treatment of retinal diseases, targeting common processes and components.
We would like to acknowledge and thank Francesco Petrillo, Carlo Gesualdo, Chiara Bianca Maria Platania and Maria Consiglia Trottafor their support on the collection’s Editorial article.
Book Synopsis Chronic Inflammation and Neurodegeneration in Retinal Disease by : Settimio Rossi
Download or read book Chronic Inflammation and Neurodegeneration in Retinal Disease written by Settimio Rossi and published by Frontiers Media SA. This book was released on 2021-12-21 with total page 135 pages. Available in PDF, EPUB and Kindle. Book excerpt: We would like to acknowledge and thank Francesco Petrillo, Carlo Gesualdo, Chiara Bianca Maria Platania and Maria Consiglia Trottafor their support on the collection’s Editorial article.
Glaucoma: A Neurodegenerative Disease of the Retina and Beyond Part B, Volume 257, the latest release in the Progress in Brain Research series, highlights new advances in the field, with this new volume presenting interesting chapters written by an international board of authors. Topics covered in this new release include Glaucoma neurodegeneration and myopia, Links between obstructive sleep apnea and glaucoma neurodegeneration, Artificial intelligence and deep learning in glaucoma: Current state and future prospects, Brain networks reorganization and functional disability in glaucoma, Advanced vascular examinations of the retina and optic nerve head in glaucoma, and much more. Covers all key aspects of current research on glaucoma Provides extensively referenced chapters, giving readers a comprehensive list of resources on topics covered Includes comprehensive and in-depth background information written in a clear form that is accessible to both specialists and non-specialists
Book Synopsis Glaucoma: A Neurodegenerative Disease of the Retina and Beyond Part B by : Giacinto Bagetta
Download or read book Glaucoma: A Neurodegenerative Disease of the Retina and Beyond Part B written by Giacinto Bagetta and published by Academic Press. This book was released on 2020-09-26 with total page 182 pages. Available in PDF, EPUB and Kindle. Book excerpt: Glaucoma: A Neurodegenerative Disease of the Retina and Beyond Part B, Volume 257, the latest release in the Progress in Brain Research series, highlights new advances in the field, with this new volume presenting interesting chapters written by an international board of authors. Topics covered in this new release include Glaucoma neurodegeneration and myopia, Links between obstructive sleep apnea and glaucoma neurodegeneration, Artificial intelligence and deep learning in glaucoma: Current state and future prospects, Brain networks reorganization and functional disability in glaucoma, Advanced vascular examinations of the retina and optic nerve head in glaucoma, and much more. Covers all key aspects of current research on glaucoma Provides extensively referenced chapters, giving readers a comprehensive list of resources on topics covered Includes comprehensive and in-depth background information written in a clear form that is accessible to both specialists and non-specialists
Glaucoma: A Pancitopatia of the Retina and Beyond, Volume 257, the latest release in the Progress in Brain Research series, highlights new advances in the field, with this new volume presenting interesting chapters written by an international board of authors. Chapters in this volume include the Genetics of glaucoma, Artificial intelligence and deep learning in glaucoma detection and monitoring, The role of commensal microflora-induced T cells responses in glaucoma neurodegeneration, Retinal cell death in experimental glaucoma, Experimental and clinical evidence on the neuroprotective properties of Citicoline in glaucoma, Glaucoma neurodegeneration and myopia, Neuronal regeneration with pluripotent stem cells in glaucoma, and more. Covers all key aspects of current research on glaucoma Provides extensively referenced chapters, giving readers a comprehensive list of resources on topics covered Includes comprehensive and in-depth background information written in a clear form that is accessible to both specialists and non-specialists
Book Synopsis Glaucoma: A Neurodegenerative Disease of the Retina and Beyond: Part A by :
Download or read book Glaucoma: A Neurodegenerative Disease of the Retina and Beyond: Part A written by and published by Elsevier. This book was released on 2020-09-22 with total page 240 pages. Available in PDF, EPUB and Kindle. Book excerpt: Glaucoma: A Pancitopatia of the Retina and Beyond, Volume 257, the latest release in the Progress in Brain Research series, highlights new advances in the field, with this new volume presenting interesting chapters written by an international board of authors. Chapters in this volume include the Genetics of glaucoma, Artificial intelligence and deep learning in glaucoma detection and monitoring, The role of commensal microflora-induced T cells responses in glaucoma neurodegeneration, Retinal cell death in experimental glaucoma, Experimental and clinical evidence on the neuroprotective properties of Citicoline in glaucoma, Glaucoma neurodegeneration and myopia, Neuronal regeneration with pluripotent stem cells in glaucoma, and more. Covers all key aspects of current research on glaucoma Provides extensively referenced chapters, giving readers a comprehensive list of resources on topics covered Includes comprehensive and in-depth background information written in a clear form that is accessible to both specialists and non-specialists
Current approaches to treat neurodegenerative disease provide only mild symptomatic relief but do not modify the natural history of these conditions. A large body of evidence suggests that mitochondrial dysfunction is a key event in the pathophysiology of neurodegeneration. Supporting and improving mitochondrial function has a big potential as a strategy for neuroprotection. The goal of this dissertation was to test whether interventions that target mitochondrial function are effective at preventing neurodegeneration induced by mitochondrial failure in vivo. A rodent model of optic neuropathy induced by the mitochondrial toxin rotenone was used to test the neuroprotective effects of methylene blue (MB) and near-infrared light (NIL), two interventions with mechanisms of action localized to mitochondria. This work also tested the effects of memantine, an NMDA receptor blocker, to further characterize the relationship between excitotoxicity and mitochondrial dysfunction. Neuroprotective effects were evaluated via behavioral testing of visual function and histopathological analysis of the retina. The neurochemical effects of MB, NIL and memantine were analyzed in vitro and in vivo with indicators of oxidative stress, cell respiration and catalytic activity of respiratory enzymes, including NADH dehydrogenase and cytochrome oxidase. MB, a diaminophenothiazine with potent antioxidant and unique redox properties, prevented the changes in visual function and the retinal histopathology induced by rotenone. In vitro, MB increased oxygen consumption and prevented the increases in oxidative stress in brain tissue induced by rotenone. NIL prevented the behavioral impairment and the decrease in retinal and visual pathway metabolic activity, retinal nerve fiber layer thickness and ganglion cell layer cell density induced by rotenone in a dose-dependent manner. Whole-brain cytochrome oxidase and superoxide dismutase activities were also increased in NIL-treated subjects in a dose-dependent manner, suggesting an in vivo transcranial effect of NIL. Finally, uncompetitive NMDA receptor blockade with memantine displayed neuroprotection against rotenone-induced neurodegeneration in a dose-response manner, and this effect was associated with a decrease in retinal oxidative stress and a long-term increase in neuronal energy metabolism capacity. These data constitute a proof-of-principle that interventions that target the mitochondria and support the function of the respiratory chain are effective at preventing neurodegeneration in vivo.
Book Synopsis Strategies of Neuroprotection in an in Vivo Model of Retinal Degeneration Induced by Mitochondrial Dysfunction by : Julio Cesar Rojas-Martinez
Download or read book Strategies of Neuroprotection in an in Vivo Model of Retinal Degeneration Induced by Mitochondrial Dysfunction written by Julio Cesar Rojas-Martinez and published by . This book was released on 2009 with total page 372 pages. Available in PDF, EPUB and Kindle. Book excerpt: Current approaches to treat neurodegenerative disease provide only mild symptomatic relief but do not modify the natural history of these conditions. A large body of evidence suggests that mitochondrial dysfunction is a key event in the pathophysiology of neurodegeneration. Supporting and improving mitochondrial function has a big potential as a strategy for neuroprotection. The goal of this dissertation was to test whether interventions that target mitochondrial function are effective at preventing neurodegeneration induced by mitochondrial failure in vivo. A rodent model of optic neuropathy induced by the mitochondrial toxin rotenone was used to test the neuroprotective effects of methylene blue (MB) and near-infrared light (NIL), two interventions with mechanisms of action localized to mitochondria. This work also tested the effects of memantine, an NMDA receptor blocker, to further characterize the relationship between excitotoxicity and mitochondrial dysfunction. Neuroprotective effects were evaluated via behavioral testing of visual function and histopathological analysis of the retina. The neurochemical effects of MB, NIL and memantine were analyzed in vitro and in vivo with indicators of oxidative stress, cell respiration and catalytic activity of respiratory enzymes, including NADH dehydrogenase and cytochrome oxidase. MB, a diaminophenothiazine with potent antioxidant and unique redox properties, prevented the changes in visual function and the retinal histopathology induced by rotenone. In vitro, MB increased oxygen consumption and prevented the increases in oxidative stress in brain tissue induced by rotenone. NIL prevented the behavioral impairment and the decrease in retinal and visual pathway metabolic activity, retinal nerve fiber layer thickness and ganglion cell layer cell density induced by rotenone in a dose-dependent manner. Whole-brain cytochrome oxidase and superoxide dismutase activities were also increased in NIL-treated subjects in a dose-dependent manner, suggesting an in vivo transcranial effect of NIL. Finally, uncompetitive NMDA receptor blockade with memantine displayed neuroprotection against rotenone-induced neurodegeneration in a dose-response manner, and this effect was associated with a decrease in retinal oxidative stress and a long-term increase in neuronal energy metabolism capacity. These data constitute a proof-of-principle that interventions that target the mitochondria and support the function of the respiratory chain are effective at preventing neurodegeneration in vivo.
This dissertation, "Neurodegeneration and Neuroprotection in Glaucoma Retinopathy-probing the Role of Endothelin-1, RAGE, A{221} and Lycium Barbarum" by Xuesong, Mi, 米雪松, 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: In order to understand the possible mechanisms in the glaucoma-related retinopathy, the role of the vasoconstrictor, endothelin-1 (ET-1), receptor for advanced glycation end-products (RAGE) as well as its ligand, Aβ in the degeneration of retinal ganglion cells (RGCs) were studied in experimental models. In addition, the relationship of ET-1, RAGE and Aβ for the RGC protective mechanism of Lycium Barbarum (LB) was also investigated. In the first part, ET-1 together with its receptors, ETA and ETB, were studied to understand their possible roles in chronic ocular hypertension (COH). The neuronal protective mechanism of LB was also determined by using a well established COH rat model. In normal rats, ET-1 and its receptors, ETA and ETB, were distributed in the retina, vasculature and optic nerve. Interestingly, ET-1 expression was up-regulated after COH. LB could decrease the expression of ET-1 and regulate its receptors (up-regulation of ETB and down-regulation of ETA in vasculature; up-regulation of ETA and down-regulation of ETB in RGCs) under the condition of COH. These data suggested that the RGC protective mechanism of LB might be related to its ability to regulate the biological effects of ET-1. To investigate the pathogenic effect of ET-1 in glaucoma, in the second part, we used transgenic mice with over-expression of ET-1 on endothelial cells (TET-1 mice). We found that beginning at 10-12 months, TET-1 mice showed a progressive retinal degeneration (loss of RGCs associated with neurons in the inner nuclear layer and outer nuclear layer of the retina) without elevation of the intraocular pressure (IOP). The data demonstrated that TET-1 mice may serve as a potential model to investigate the role of endothelial ET-1 in the pathogenesis of normal tension glaucoma and other degenerative retinopathy. To investigate whether LB plays a role on neuronal protection other than in COH, in the third part, we used an acute ocular hypertension (AOH)-induced ischemia mouse model. We found that LB could rescue RGCs under AOH insult, associating with blood vessel protection (decreasing the damage of blood-retinal-barriers and rescuing the survival of endothelial cells and pericytes) and inhibiting retinal gliosis. We also found the protective mechanism of LB was closely correlated with down-regulation of the expression of RAGE, ET-1, APP (amyloid precursor protein), AGE (advanced glycation end-product) as well as Aβ; therefore to reduce the damage effects of these RAGE-mediated reactions to the retinal neurons, blood vessels and glial cells involved in the ischemic insult. Taken together, the present study demonstrated that TET-1 mice may be a potential model for investigating the role of ET-1 in degenerative retinopathies, such as normal tension glaucoma. We also showed the neuronal protective mechanism of LB in vivo was associated with inhibiting the biological effect of ET-1 and down-regulating the damage signaling pathways mediated by the activation of RAGE and its ligands (AGE and Aβ). These results provided further understandings in the mechanism of the glaucoma-related retinopathy. In addition, LB could be a neuroprotective agent to the retina following both chronic and acute injuries. DOI: 10.5353/th_b4724392 Subjects: Neuroprotective agents Lycium chinense - Therapeutic use En
Book Synopsis Neurodegeneration and Neuroprotection in Glaucoma Retinopathy-Probing the Role of Endothelin-1, Rage, A{221} and Lycium Barbarum by : Xuesong Mi
Download or read book Neurodegeneration and Neuroprotection in Glaucoma Retinopathy-Probing the Role of Endothelin-1, Rage, A{221} and Lycium Barbarum written by Xuesong Mi and published by Open Dissertation Press. This book was released on 2017-01-26 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: This dissertation, "Neurodegeneration and Neuroprotection in Glaucoma Retinopathy-probing the Role of Endothelin-1, RAGE, A{221} and Lycium Barbarum" by Xuesong, Mi, 米雪松, 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: In order to understand the possible mechanisms in the glaucoma-related retinopathy, the role of the vasoconstrictor, endothelin-1 (ET-1), receptor for advanced glycation end-products (RAGE) as well as its ligand, Aβ in the degeneration of retinal ganglion cells (RGCs) were studied in experimental models. In addition, the relationship of ET-1, RAGE and Aβ for the RGC protective mechanism of Lycium Barbarum (LB) was also investigated. In the first part, ET-1 together with its receptors, ETA and ETB, were studied to understand their possible roles in chronic ocular hypertension (COH). The neuronal protective mechanism of LB was also determined by using a well established COH rat model. In normal rats, ET-1 and its receptors, ETA and ETB, were distributed in the retina, vasculature and optic nerve. Interestingly, ET-1 expression was up-regulated after COH. LB could decrease the expression of ET-1 and regulate its receptors (up-regulation of ETB and down-regulation of ETA in vasculature; up-regulation of ETA and down-regulation of ETB in RGCs) under the condition of COH. These data suggested that the RGC protective mechanism of LB might be related to its ability to regulate the biological effects of ET-1. To investigate the pathogenic effect of ET-1 in glaucoma, in the second part, we used transgenic mice with over-expression of ET-1 on endothelial cells (TET-1 mice). We found that beginning at 10-12 months, TET-1 mice showed a progressive retinal degeneration (loss of RGCs associated with neurons in the inner nuclear layer and outer nuclear layer of the retina) without elevation of the intraocular pressure (IOP). The data demonstrated that TET-1 mice may serve as a potential model to investigate the role of endothelial ET-1 in the pathogenesis of normal tension glaucoma and other degenerative retinopathy. To investigate whether LB plays a role on neuronal protection other than in COH, in the third part, we used an acute ocular hypertension (AOH)-induced ischemia mouse model. We found that LB could rescue RGCs under AOH insult, associating with blood vessel protection (decreasing the damage of blood-retinal-barriers and rescuing the survival of endothelial cells and pericytes) and inhibiting retinal gliosis. We also found the protective mechanism of LB was closely correlated with down-regulation of the expression of RAGE, ET-1, APP (amyloid precursor protein), AGE (advanced glycation end-product) as well as Aβ; therefore to reduce the damage effects of these RAGE-mediated reactions to the retinal neurons, blood vessels and glial cells involved in the ischemic insult. Taken together, the present study demonstrated that TET-1 mice may be a potential model for investigating the role of ET-1 in degenerative retinopathies, such as normal tension glaucoma. We also showed the neuronal protective mechanism of LB in vivo was associated with inhibiting the biological effect of ET-1 and down-regulating the damage signaling pathways mediated by the activation of RAGE and its ligands (AGE and Aβ). These results provided further understandings in the mechanism of the glaucoma-related retinopathy. In addition, LB could be a neuroprotective agent to the retina following both chronic and acute injuries. DOI: 10.5353/th_b4724392 Subjects: Neuroprotective agents Lycium chinense - Therapeutic use En
Neuroprotection is a strategy to prevent or delay the progression of chronic neurodegenerative diseases, acute neurological disorders, or even mental disorders. The major aim of this book is to focus on different approaches to achieve neuroprotection. In this book, there are chapters discussing imidazoline ligands and opioid ligands in Alzheimer's disease, the beneficial effects of adenosine A2A receptor antagonist, adrenergic receptor agonists and antagonists modulating microglial responses, and different approaches to achieve neuroprotection against aging-associated macular degeneration. This book will give insights to scientists in the field to stimulate their research, medical professionals to review their clinical practices, and others who would like to learn more about different neuroprotective approaches.
Book Synopsis Neuroprotection by : Raymond Chuen-Chung Chang
Download or read book Neuroprotection written by Raymond Chuen-Chung Chang and published by BoD – Books on Demand. This book was released on 2019-08-28 with total page 104 pages. Available in PDF, EPUB and Kindle. Book excerpt: Neuroprotection is a strategy to prevent or delay the progression of chronic neurodegenerative diseases, acute neurological disorders, or even mental disorders. The major aim of this book is to focus on different approaches to achieve neuroprotection. In this book, there are chapters discussing imidazoline ligands and opioid ligands in Alzheimer's disease, the beneficial effects of adenosine A2A receptor antagonist, adrenergic receptor agonists and antagonists modulating microglial responses, and different approaches to achieve neuroprotection against aging-associated macular degeneration. This book will give insights to scientists in the field to stimulate their research, medical professionals to review their clinical practices, and others who would like to learn more about different neuroprotective approaches.
