Animal Models Of Retinal Degeneration

Affecting over a hundred million individuals worldwide, retinal diseases are among the leading causes of irreversible visual impairment and blindness, and appropriate study models, especially animal models, are essential to furthering our understanding of the etiology, pathology, and progression of these endemic diseases. In Animal Models for Retinal Diseases, recognized experts in the field highlight valuable techniques as well as animal models for the prominent retinal diseases in order to aid in the evaluation, development, and improvement of therapeutic strategies. Beginning with an overview of the morphology of the retina, visual behavior, and genetics and genomics approaches for retinal research, the book continues by covering animal models for the research of specific human retinal diseases, e.g., retinal degeneration, age-related macular degeneration, retinopathy of prematurity, diabetic retinopathy, glaucoma, retinal ischemia, and retinal inflammation. As a volume in the successful Neuromethods series, the chapters provide authoritative reviews of the most commonly used approaches in the field. Vital and easy to use, Animal Models for Retinal Diseases serves to support the important future research of ocular investigators, ophthalmologists, and neuroscientists currently delving into this fascinating field of study.

Age-related macular degeneration (AMD) is a degenerative condition that begins in Bruch’s membrane and progresses to involve the retinal pigment epithelium and ultimately, overlying photoreceptors. The only required etiologic factor is age, and AMD is regarded as the leading cause of blindness in individuals over 65 years. AMD results from variable contributions of age, environment, and genetic predisposition. Many loci are linked to AMD—in the vast majority of cases, the disease is associated with polymorphisms within these genes, rather than mutations that ablate gene function. The etiologic complexity of AMD is reflected by the paucity of animal models that entirely replicate the human disease. In this review, we compare the salient anatomy of the primate and rodent retina, particularly in the light of AMD pathology. Next, prevailing hypotheses explaining how AMD may develop are discussed. These include the role of complement activation and macrophage chemotaxis in AMD, molecular mechanisms of choroidal neovascularization, and the roles of oxidative damage and lipid metabolism. An overview of spontaneous and induced non-human primate models is given, and relevant mouse models are described in the context of each pathogenetic mechanism.

Photobiomodulation in the Brain: Low-Level Laser (Light) Therapy in Neurology and Neuroscience presents the fundamentals of photobiomodulation and the diversity of applications in which light can be implemented in the brain. It will serve as a reference for future research in the area, providing the basic foundations readers need to understand photobiomodulation’s science-based evidence, practical applications and related adaptations to specific therapeutic interventions. The book covers the mechanisms of action of photobiomodulation to the brain, and includes chapters describing the pre-clinical studies and clinical trials that have been undertaken for diverse brain disorders, including traumatic events, degenerative diseases and psychiatric disorders. Provides a much-needed reference on photobiomodulation with an unprecedented focus on the brain and its disorders Features a body of world-renowned editors and chapter authors that promote research, policy and funding Discusses the recent and rapid accumulation of literature in this area of research and the shift towards the use of non-invasive techniques in therapy

Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases in humans characterized by the loss of photoreceptor cells leading to reduction of the peripheral visual field (known as tunnel vision) and eventually to blindness. N-Methyl-N-nitrosourea (MNU) is an alkylating agent that exhibits its toxicity by transferring its methyl group to nucleobases in nucleic acids. A single systemic administration of MNU causes retinal degeneration in various animal species. The retinal degeneration is highly reproducible, and the photoreceptor cell loss occurs within a week when a suitable dose of MNU is administered. Photoreceptor cell loss occurs via apoptosis, which resembles human RP. Decreased levels of basal autophagy concomitantly occur during the course of apoptosis progression. The time-course progression of the disease, the molecular mechanisms of the disease, and the therapeutic trials against MNU-induced photoreceptor cell apoptosis are described.

This book presents new and noteworthy research into retinal diseases. It focuses on what we currently know about the environment, genetics and mechanisms that lead to retinal degenerations, new diagnostics, and innovative therapeutic modalities to preserve vision. Written by renowned scientific investigators, this innovative collection of treatment strategies and technological discoveries allows for the realistic translation of research into practice.

This book will contain the proceedings of the XIV International Symposium on Retinal Degeneration (RD2010), held July 13-17, 2010, in Mont-Tremblant, Quebec, Canada. The volume will present representative state-of-the-art research in almost all areas of retinal degenerations, ranging from cytopathologic, physiologic, diagnostic and clinical aspects; animal models; mechanisms of cell death; candidate genes, cloning, mapping and other aspects of molecular genetics; and developing potential therapeutic measures such as gene therapy and neuroprotective agents for potential pharmaceutical therapy.