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This book focuses on the physiology and molecular biology of the front and back regions of the eye. Specifically, the chapters of this book cover topics that explain currently less understood aspects of retinal health as well as the use of zebrafish models to understand the molecular pathogenesis of associated diseases. This includes retinitis pigmentosa, diabetic retinopathy ciliopathies in the eye, rhodopsin trafficking and associated disorders, and the biochemistry of cone defects. This book serves as a useful reference for scientists and graduate students seeking to understand protein trafficking mechanisms and metabolic control in retinal diseases.
There are more than 300 genes that have been identified which carry mutations that cause various forms of retinal dysfunction and degeneration, making the study of retinal diseases a subject of high relevance. In this compendium of original and review articles, many of the diseases and pathways associated with disorders of the retina are examined using animal models, to provide the reader with a good overview of current retinal research. Within this volume, you will find research reports on many of the most prominent retinal disorders, such as diabetic retinopathy (DR), age-related macular degeneration (AMD), choroidal neovascularization (CNV), and retinitis pigmentosa (RP). We hope that the work presented here will stimulate new ideas and lead to effective treatments for retinal diseases.
As the average life expectancy of many populations throughout the world increases, so to does the incidence of such age-related neurodegenerative disorders as Alzheimer's, Parkinson's, and Huntington's diseases. Rapid advances in our understanding of the molecular genetics and environmental factors that either cause or increase risk for age-related neurodegenerative disor ders have been made in the past decade. The ability to evaluate, at the cellular and molecular level, abnormalities in postmortem brain tissue from patients, when taken together with the development of valuable animal and cell-culture models of neurodegenerative disorders has allowed the identification of sequences of events within neurons that result in their demise in specific neurodegenerative disorders. Though the genetic and environmental factors that pro mote neurodegeneration may differ among disorders, shared biochemical cascades that will ultimately lead to the death of neurons have been identified. These cascades involve oxyradical production, aberrant regulation of cellular ion homeostasis and activation of a stereotyped sequence of events involving mitochondrial dysfunction and activa tion of specific proteases. Pathogenesis of Neurodegenerative Disorders provides a timely compilation of articles that encompasses fundamental mechanisms involved in neurodegenerative disorders. In addition, mechanisms that may prevent age-related neurodegenerative disorders are presented. Each chapter is written by an expert in the particular neurodegenerative disorder or mechanism or neuronal death discussed.
Humans, like many other vertebrates, possess five Aristotelian senses (vision, olfaction, hearing, taste, and touch) which we use to experience and navigate our environment. Our visual system is the only source of light detection and light signaling in our bodies. This makes our visual system essential for detecting movement, distance, time of day, and seasonal changes in the length of days within our environment. The visual systems of most animals are designed to capture photons of visible light and convert that energy into a neurological signal (visual signal) to be transmitted to brain regions responsible for visual perception1 . This visual signaling allows animals to navigate and respond to any immediate changes or threats in their environment. In addition, visual signaling to the brain also regulates many non-image forming involuntary behaviors. For example, humans are able to entrain some behavioral and physiological activity to the day/night cycles. Activities such as sleep, melatonin biosynthesis, heart rate, and body temperature all rely on visual input to modify their activity in accordance with day/night light cycles1 . In this way our visual system broadly affects our daily activities and the efficiency at which we perform those activities. Recent estimates suggest that 4.2 million Americans over the age of 40 suffer from an uncorrectable visual impairment2,3. In addition, it was estimated that 2.2 million children and adults under the age of 40 suffer from uncorrectable vision loss, including blindness4 . The identification of this population and the understanding that the number of individuals with these conditions will continue to increase as our population continues to age. It is imperative that new models for treatment are developed to promote better prognosis and restore function within this population. Our lab is interested in describing the molecular mechanisms that underlie photoreceptor cell death and vision loss within a retinal degenerative disease, Mucolipidosis type IV (MLIV). Uncovering the mechanisms that result in photoreceptor x pathogenesis can lead to developing novel target therapeutic approaches to rescue the loss of visual function.
Neurodegeneration is characterized by the progressive loss of neural tissue that result in various neurodegeneration-initiated cerebral failures and complex diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease. All these medical conditions are accompanied by the disruption of blood-brain barrier (BBB). The BBB is an interface, separating the brain from the circulatory system and protecting the central nervous system from potentially harmful chemicals while regulating transport of essential molecules and maintaining a stable environment. Owing to the inability of the neurons to regenerate on their own after neurodegeneration or severe damage to the neural tissue, neurodegenerative disorders do not have natural cures on their own. Neuroregeneration is a viable way to curb neurodegeneration. One of the current approaches is stem cell-based therapy that has been shown to be potentially helpful for the application of neuronal cell replacement for neuroregeneration. It is vital that the neurodegenerative disorder being detected at an early stage as it can provide a chance for treatment that may be helpful to prevent further progression of the fatal disease. Thus, research has focused on developing effective non-invasive diagnostic methods for early detection of these disorders. Molecular diagnostics can provide a powerful method to detect and diagnose various neurological disorders. Such diagnosis can enhance early detection, provide subsequent medical counsel based on medical pathway, as well as to gain better insight of neurogenesis and hopefully eventual cure of the neurodegenerative diseases. With research reports, reviews, mini-reviews and commentary, this research topic covers a wide range of areas in neurodegeneration research, including diagnosis and prognosis; regulating central nervous system; biomarkers and brain injury induced neurobehavioral outcomes among other timely reports on neurodegeneration.
The editor of this volume, having research interests in the field of ROS production and the damage to cellular systems, has identified a number of enzymes showing ·OH scavenging activities details of which are anticipated to be published in the near future as confirmatory experiments are awaited. It is hoped that the information presented in this book on NDs will stimulate both expert and novice researchers in the field with excellent overviews of the current status of research and pointers to future research goals. Clinicians, nurses as well as families and caregivers should also benefit from the material presented in handling and treating their specialised cases. Also the insights gained should be valuable for further understanding of the diseases at molecular levels and should lead to development of new biomarkers, novel diagnostic tools and more effective therapeutic drugs to treat the clinical problems raised by these devastating diseases.
Over the past decades, knowledge about the cellular and molecular basis underlying the visual process has remarkably increased. In Retinal Degeneration: Methods and Protocols, expert researchers in the field provide a guide of relevant and state-of-the-art methods for studying retinal homeostasis and disease. These include methods and techniques for addressing cell culture systems and animal models of disease, their generation, their phenotypic and molecular characterization as well as their use in therapeutic approaches to the retina. Written in the highly successful Methods in Molecular BiologyTM series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and key tips on troubleshooting and avoiding known pitfalls. Authoritative and practical, Retinal Degeneration: Methods and Protocols aids scientists in continuing to study the cutting-edge techniques of retinal cell biology in health and disease.
Neurodegenerative disorders are characterized by progressive atrophy and dysfunction of anatomically or physiologically related neurologic systems. There are several common features of neurodegenerative disorders. They are mostly chronic, progressive and start due to the death of specific neuronal populations in the central nerve system (CNS). The distinct clinical phenotypes are generally linked to neuronal loss and often associated with aging. These disorders might share common pathogenetic mechanisms such as intracytoplasmic or intranuclear inclusions in neurons or glia which are linked to the intracellular deposition of abnormal misfolded protein aggregates. The upsurge in longevity is accelerating. The Baby Boomers turned 60 in 2006, and are part of the rapid growth in the aging population in the United States and worldwide. Nearly 36 million people in the United States are aged 65 or older, and life expectancy at birth has reached 77.5 years compared with 3 million in 1900 with life expectancy of 47.3. Most notable is the growth in the population of individuals age 85 and older when neurodegenerative diseases are prevalent. Indeed, these disorders affect increasing populations and it is estimated, for example, that around 4.5 million Alzheimer's patients are living in the United States. In this book, we focus on the major and most common neurodegenerative disorders namely, Alzheimer s (AD), Parkinson s diseases (PD), multiple system atrophy (MSA), Huntington s disease (HD) and amyotrophic lateral sclerosis (ALS). We also included the less common, but clinically and scientifically most interesting occurrance, the prion diseases. In addition to the description of the pathophysiology and the molecular basis of the inherited and sporadic phenomena we tried to illustrate the common basis for this range of clinical conditions. One of the shared histological features of many neurodegenerative diseases is the accumulation of misfolded proteins. The aggregated proteins, such as alpha-synuclein and synphilin-1 in PD, and beta-amyloid (Ab) and tau in AD affect neuronal connectivity and plasticity, and trigger cell death signaling pathways. The inclusions observed in PD are called Lewy bodies and are found mostly in the cytoplasm. AD brains show intracellular neurofibrillary tangles, which contain tau, and extracellular plaques, which contain Ab. Other illnesses with inclusions are Huntington s (polyQ), ALS, and prion diseases. The intra- or extracellular protein aggregates are thought to accumulate in the brain as a result of a decrease in molecular chaperone or proteasome activities which are used as cellular quality control systems. In fact, several mutations that disturb the activity of molecular chaperones or the ubiquitin-proteasome system associated enzymes, can cause neurodegeneration. It has been suggested that either genetic mutations or an increase in nitrosative/oxidative stress can facilitate protein aggregation. A growing body of evidence indicates that neurodegenerative processes in general, are associated with oxidative stress. These data lead to the convincing idea that several neurological disorders may be prevented and/or cured by antioxidant properties. Therefore, one of the chapters review some aspects related to the role of antioxidants in neurodegenerative diseases. The emerging concept of regenerative medicine holds great promise for the numerous patients suffering from various ailments of the nervous system. The last chapter focuses on the adult stem cells residing in the bone marrow being a possible remedy for some of the nervous system diseases. Whether through cell replacement, cell restoration or gene delivery, bone marrow stem cells allow physicians to perform autologous cell transplantation, thus avoiding immune rejection, a major obstacle of cellular therapy.
This comprehensive reference provides a detailed overview of current concepts regarding the cause of Parkinson's disease-emphasizing the issues involved in the design, implementation, and analysis of epidemiological studies of parkinsonism.
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