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As clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing, attention has turned to the brain's own endogenous strategies for neuroprotection. Two endogenous mechanisms have been recently characterized, ischemic preconditioning and ischemic postconditioning. In the present topic newly characterized mechanisms involved in preconditioning- and postconditioning- neuroprotection will be discussed. The understanding of the mechanisms involved in the neuroprotective pathways induced by preconditioning and postconditioning will be clinically relevant for identifying new druggable target for neurodegenerative disorder therapy. Furthermore, the importance of these neuroprotective strategies resides in that it might be easily translatable into clinical practice. Therefore, the data presented here will highlight the capacity of ischemic preconditioning and postconditioning to be of benefit to humans.
As clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing, attention has turned to the brain's own endogenous strategies for neuroprotection. Two endogenous mechanisms have been recently characterized, ischemic preconditioning and ischemic postconditioning. In the present topic newly characterized mechanisms involved in preconditioning- and postconditioning- neuroprotection will be discussed. The understanding of the mechanisms involved in the neuroprotective pathways induced by preconditioning and postconditioning will be clinically relevant for identifying new druggable target for neurodegenerative disorder therapy. Furthermore, the importance of these neuroprotective strategies resides in that it might be easily translatable into clinical practice. Therefore, the data presented here will highlight the capacity of ischemic preconditioning and postconditioning to be of benefit to humans.
Cerebral preconditioning is a phenomenon wherein a mild insult or stress induces cellular and tissue adaptation or tolerance to a later, severe injury, therefore reflecting the efficacy of endogenous mechanisms of cerebrovascular protection. Initially identified for rapid cardiac protection, preconditioning has expanded to all aspects of CNS protection from ischemia, trauma and potentially neurodegeneration. Many different stimuli or stressors have been identified as preconditioning agents, suggesting a downstream convergence of mechanisms and underscoring the potential for translational application of preconditioning in the clinic. Moreover, the fundamental mechanisms responsible for preconditioning-induced tolerance will help in the design novel pharmacological approaches for neuroprotection. While stroke and many other brain injuries are not predictable, in some populations (e.g., metabolic syndrome, patients undergoing carotid endarterectomy, aneurysm clipping, or with recent TIAs) the risk for stroke is identifiable and significant, and preconditioning may represent a useful strategy for neuroprotection. For unpredictable injuries, post-conditioning the brain – or inducing endogenous protective mechanisms after the initial injury – can also abrogate the extent of injury. Finally, remote pre- and post-conditioning methods have been developed in animals, and are now being tested in clinical trials, wherein a brief, noninjurious stress to a noncerebral tissue (i.e., skeletal muscle) can provide protection to the CNS and thereby allows clinicians the opportunity to circumvent concerns regarding the direct preconditioning of neurological tissues.
Traumatic brain injury (TBI) remains a significant source of death and permanent disability, contributing to nearly one-third of all injury related deaths in the United States and exacting a profound personal and economic toll. Despite the increased resources that have recently been brought to bear to improve our understanding of TBI, the developme
Neurological disease affects nearly 25%–30% of the world’s population, exerting enormous financial strain on the healthcare system. Estimated current costs are around $800 annual billion, and this number is expected to increase exponentially as the global population ages. As such, new and alternative neuroprotective strategies are urgently needed. This book examines some of the most promising approaches in neuroprotection as well as discusses current goals and prospects. Organized into three sections, chapters cover such topics as the use of cannabinoids, medicinal plants, and essential oils in Alzheimer’s and Parkinson’s; protein misfolding and the neuroprotective potential of vitamin E in cerebral ischemia; and potential new neurological treatments and their mechanisms of action.
Target pattern recognition in innate immunity is responsible for the immediate, usually protective, responses shown against invading microorganisms, and it is the principal feature of self and non-self recognition by virtue of the recognition of structures on the microbial pathogens, which are not found on host cells. This is an area that has been very actively researched, over approximately the past 12 years, and therefore this volume provides a timely comprehensive, and up to date, summary of the types and range of cell surface, intracellular, and secreted, host proteins involved in the recognition of microbial products, and of the protective mechanisms triggered as a result of the recognition events. The Toll-like receptors, first described in Drosophila and now well-characterised on human cells, provide an excellent demonstration of the wide range of different microbial products recognised by this family of receptors and of the signalling pathways which are triggered thus leading to induction of inflammatory cytokines and the activation of genes producing antimicrobial products. In addition, several cell surface proteins involved in target pattern recognition have been described on the surfaces of macrophages (macrophage mannose receptor and macrophage scavenger receptors), and on dendritic cells (DEC205), and to be involved with the uptake and clearance of whole microorganisms and polyanioic ligands. Pattern recognition is also utilised by intracellular receptors, with NOD-like receptors in the cytosol recognizing microbial molecules and activating the production of inflammatory cytokines or pathways that induce the production of inflammatory molecules. Secreted proteins, such as the pentraxins, which includes the acute phase reacting, C-reactive protein (CRP) and serum amyloid protein (SAP), and the collectins (mannan binding lectin, lung surfactant protein A and D) and ficolins can also readily recruit killing and clearance systems. Indeed, the serum complement system, which is one of the major defence systems in the bloodstream, is efficiently activated by CR P on its binding to the phosphocholine groups of microbial phospholipids—and the subsequent interaction of the bound CR P with C1q—to give classical pathway activation, or MBL, or ficolin, binding to arrays of mannose or N-acetyl-glucosamine residues, respectively, on the surfaces of microorganisms—to give lectin pathway activation. Also, in addition to the activation and clearance events associated with complement activation by some of the secreted pattern recognition receptors, it is accepted that all these pattern recognition receptors can generally accelerate the uptake and clearance of microbes via phagocytic cells. In view of the growing interest in the cross-talk between innate and adaptive immunity, a thorough understanding of the initial recognition and triggering events, mediated via innate immune receptors, as addressed in this volume, is clearly very useful in helping to also fully understand the mechanisms of activation and control of the adaptive immune system—and to allow a full assessment of the relative roles played by innate immunity and adaptive immunity against a particular infection in higher organisms.
A critical and comprehensive look at current state-of-the-art scientific and translational research being conducted internationally, in academia and industry, to address new ways to provide effective treatment to victims of ischemic and hemorrhagic stroke and other ischemic diseases. Currently stroke can be successfully treated through the administration of a thrombolytic, but the therapeutic window is short and many patients are not able to receive treatment. Only about 30% of patients are "cured" by available treatments. In 5 sections, the proposed volume will explore historical and novel neuroprotection mechanisms and targets, new and combination therapies, as well as clinical trial design for some of the recent bench-side research.
A translational overview of neuroimmune diseases for neuroscientists and clinicians that clarifies the pathological mechanisms underlying neuroimmune diseases and builds a comprehensive bridge between the latest research findings and their clinical implications in daily practice. The material is presented in two steps. The first section comprises a review of the pathogenic actions of immune cells in brain diseases. Here the authors discuss the mechanisms through which immune cells disrupt the functions of nerve cells. The second section explores the ways in which the brain becomes dysfunctional due to impaired nerve cell function. Based on pathogenesis, diagnostic and therapeutic strategies are discussed for each clinical category. The book will be invaluable for use in clinical practice of neuroimmune diseases
This fully revised edition explores the management of neurological disorders with a focus on neuroprotection, disease modification, and neuroregeneration rather than symptomatic treatment. Since the publication of the first edition, advances in biotechnology, particularly in cell and gene therapies, are reflected in this volume, as are numerous new and repurposed drugs in clinical trials. Overall, The Handbook of Neuroprotection serves as a comprehensive review of neuroprotection based on knowledge of the molecular basis of disorders of the central nervous system. In-depth and authoritative, The Handbook of Neuroprotection, Second Edition features a compendium of vital knowledge aimed at providing researchers with an essential reference for this key neurological area of study.