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This book is about the'Mechanism and Genetic susceptibility of Neurological disorders. It is a comprehensive exploration, penned by esteemed authors, and offers a profound understanding of these enigmatic ailments, their progression, and the strategic approaches employed to mitigate their impact. In this book, readers will uncover a wealth of knowledge surrounding the mechanistic intricacies that underlie various neurological disorders. Through meticulous research and insightful analysis, the authors elucidate the inner workings of these conditions, shedding light on the mechanisms responsible for their onset and progression. The central themes of this book are the recognition of the genetic landscape governing neurological disorders. It emphasizes the role played by a diverse array of genes in the development and progression of these conditions, highlighting the multifaceted genetic susceptibility that underlies their manifestation. ​

The aim of the book is to sensitize physicians and researchers to the important long-term health effects of early, persistent, and severe trauma. The author, an internist, rheumatologist, and basic researcher in psychoneuroimmunology, shows connections between adverse childhood experiences and typical adult sequelae. After early traumatic experiences and childhood stress, there is a higher incidence of mental illness, chronic pain, sleep disorders, dental problems, obesity, cardiovascular disease, asthma, diabetes mellitus and chronic inflammation. A selection of diseases unmistakably demonstrate the long-term consequences of early childhood trauma. These childhood experiences create a kind of long-term programming that has a negative effect in adulthood. From his psychoneuroimmunological perspective, Rainer Straub identifies four factors that link the brain to the immune system and are involved in chronic immune activation: direct connectors originating from the brain, indirect connectors functioning through hormonal and neuronal pathways, extracorporeal (the environmental factors) and pleiotropic connectors (genetic factors).The translation was done with the help of artificial intelligence. A subsequent human revision was done primarily in terms of content.

Neuroinflammation in Vascular Dementia describes the molecular mechanisms that drive this transition to mixed pathology, along with the newer lifestyle and pharmacological approaches that can reduce the incidence of dementia. The book describes the practical aspects of neuroimaging methods, along with novel neuroimaging methods, using MRI, that are becoming important clinically. The author also discusses how the diagnosis of dementias will be greatly aided by biomarkers from neuroimaging, blood and CSF biochemistry and neuropsychological testing in the future. This information will be used in precision medicine to design treatment strategies based on the most likely causes of the disease. Dementia research has undergone dramatic growth driven by current and projected increases in the aging of the population, and thus leading to a larger number of patients with dementia by 2050. Hence, advances in neuroimaging, brain chemistry, and genetics have accelerated our understanding of diseases that lead to cognitive decline. - Reviews the clinical aspects and subtypes of dementia - Explains molecular pathways involved in brain inflammation - Includes the role of CSF and blood in diagnosis - Covers established and novel neuroimaging methods - Discusses established and developing treatment strategies - Identifies future directions, such as machine learning and precision medicine

Role of Inflammation in Environmental Neurotoxicity, Volume Three, in this comprehensive serial, addresses contemporary advances in neurotoxicology by providing authoritative review articles on key issues in the field. Edited by leading subject experts, topics of note in this new release include Neuroinflammation (Introduction), Organophosphates, Lead, Manganese, Drugs of abuse, Peripheral vs central inflammation, Air pollution, Developmental neurotoxicity, Ethanol, and the Blood brain barrier, amongst other topics. - Provides a unique, first of its kind resource - Contributed to by world leaders in neurotoxicology - Contains a diversity of topics (from molecular to epidemiology) in neurotoxicology

Late aging associated changes in alcohol sensitivity, neurobehavioral function, and neuroinflammation, Volume 148, the latest release in the International Review of Neurobiology series, highlights new advances in the field, with this new volume presenting interesting chapters on a variety of timely topics. Each chapter is written by an international board of authors. - Provides the authority and expertise of leading contributors from an international board of authors - Presents the latest release in the International Review of Neurobiology series - Includes the latest information on late aging-associated changes in alcohol sensitivity, inflammation and cognitive decline

Inflammation and Immunity in Depression: Basic Science and Clinical Applications is the first book to move beyond the established theory of cytokine-induced depression and explore the broader role the immune system plays in this devastating mood disorder. The book fully explores the most recent lines of research into this rapidly advancing field, including alterations of T-cells, the neurobiological implications of neuroinflammation and immune alterations for brain development and function, and the genetic components of neuroinflammation in depression, including the relationships between stress and inflammation that are revealing gene-environment interactions in the disorder. Combining contributions from researchers worldwide, this book provides the most comprehensive discussion available today on the involvement of the innate immune and adaptive immune systems in depressive disorder. Chapters span neuroscience, psychology, clinical applications and future directions, making this book an invaluable resource for advanced students, researchers and practitioners who need to understand the complex and varied role of inflammation and immune responses in depression. - Synthesizes current knowledge of inflammation and immunity in depression, ranging from basic neuroscience research, to clinical applications in psychiatry - Expands on the long-established theory of cytokine-induced depression to discuss broader involvement of the immune system - Explores translational potential of targeting immune dysfunction for clinical interventions

This PIR volume presents a comprehensive collection of reviews that focus on the role of the blood-brain barrier (BBB) during steady-state and inflamed conditions. Within the central nervous system (CNS) the constantly changing bloodstream is strictly separated from the CNS parenchyma by the BBB. However, viruses, bacteria, parasites and auto-aggressive immune cells can penetrate the barrier and significantly contribute to CNS inflammation. The BBB can actively contribute to neuroinflammation by presentation of chemokines, expression of cell adhesion molecules and alterations of barrier properties. As such, understanding the role of the BBB under healthy and pathological conditions is essential to the development of new drugs to efficiently combat inflammatory diseases of the CNS.

Inflammation has invaded the field of psychiatry. The finding that cytokines are elevated in various affective and psychotic disorders brings to the forefront the necessity of identifying the precise research domain criteria (RDoCs) that inflammation is responsible for. This task is certainly the most advanced in major depressive disorders. The reason is that a dearth of clinical and preclinical studies has demonstrated that inflammation can cause symptoms of depression and conversely, cytokine antagonists can attenuate symptoms of depression in medical and psychiatric patients with chronic low grade inflammation. Important knowledge has been gained on the symptom dimensions that inflammation is driving and the mechanisms of action of cytokines in the brain, providing new targets for drug research and development. The aim of the book “Inflammation-Associated Depression” is to present this field of research and its implications in a didactic and comprehensive manner to basic and clinical scientists, psychiatrists, physicians, and students at the graduate level.

This unifying theme of this book-with sections on mechanisms of defense and neuropathogenesis, neurological diseases, infections of the nervous system, neuropharmacology, and novel therapies-is interactions of the immune and nervous systems. It also discusses the role of inflammation as a key mediator of different brain disorders. There have been significant scientific advances in the multidisciplinary field of neuroimmunology / neuroinflammation in the past decade, and this book, edited under the guidance of Professor P. N. Tandon, fosters communication between those who share an interest in this exciting area, including neuroscientists, immunologists, cell biologists, clinicians and neuropharmacologists.

Unless new discoveries are made in the prevention or treatment of stroke, Alzheimer's Disease and depression, the number of patients with these diseases is sure to increase dramatically by the year 2050. Thus, developing strategies to retard or delay the onset of stroke, AD and depression these neurological disorders is of critical important. The present monograph will provide current and comprehensive information on the relationship between neuroinflammation and oxidative stress in age-related neurological disorders at the molecular level. The information described in this monograph on lifestyle (diet and exercise), genes and age is intended to facilitate and promote new discoveries for the treatment of age-related neurological disorders.

State of the art reviews by experts in the fields of neuroscience, immunology, microbiology/infectious diseases and pharmacology addressing the convergence of the immune system (neuroinflammation) and the loss of neurons (neurodegeneration). Many of the diseases that are discussed in the book are of epidemic proportion, e.g., Alzheimer's disease, Parkinson's disease, stroke, viral encephalitides and substance abuse. In addition to discussions of the involvement of neuroinflammation and neurodegeneration in these disorders, scientific reviews are presented on the cells and mediators that participate in defense of and damage to the nervous system. With rare exception, no or inadequate treatment exists for the diseases discussed in this book. An underlying premise of the book is that understanding of their shared pathogenic mechanisms will lead to improved therapies. Given the rapid evolution of the field of Neuroimmune Pharmacology, readers will find this book to be the most timely and authoritative reference on the subject of each of its chapters.

Accumulation on glia is an active pathological element in many neurological disorders. Gliosis produces neuroinflammation through both neurotrophic and inflammatory means, but the exact mechanism through which this happens remain unclear. It is suspected that damage to neurons activates the growth of glial cells. The proposed book focuses on the interaction between neurons and glia to help elucidate the pathophysiology of neuroinflammation in neurological disorders.​

A Primer of Neuroimmunological Disease is a significant new resource for anyone interested in conditions such as multiple sclerosis(MS), myasthenia gravis, and neurological infections. It is a practical and balanced guide to the diagnosis and treatment of neuroimmunological disease. A Primer of Neuroimmunological Disease distinguishes itself by providing a range of features not generally included in texts on neuroimmunology. These include broad presentation of information in the form of figures and tables; strong cohesion among topics by focusing on a few prototypic neuroimmunological diseases, which serve as a foundation from which to explore other neuroimmunological diseases; a single author perspective, with references across chapters; and a focus on the overlap between neuroimmunological and neuroinfectious diseases. Neurologists, immunologists, infectious disease specialists, neuroscientists and others interested in neuroimmunological diseases such as MS will find A Primer of Neuroimmunological to be a state-of-the-art resource.

Up until approximately 20 years ago, the idea that the central nervous system (CNS) and components of the immune system were dynamically interactive was considered impossible (or at least highly unlikely) as the CNS was judged an immunosuppressive environment based upon experimental evidence highlighting the survival of tissue grafts within the brain. Additional evidence supporting this viewpoint included (i) the presence of the blood–brain barrier (BBB) which p- vides a physical and physiological obstruction that is difficult for cells and mac- molecules to cross, (ii) the relative absence of MHC class I and II expression on CNS cells like astrocytes and neurons, and (iii) lack of abundant antigen presenting cells (APC) which are required for the generation of an adaptive immune response. However, in spite of these obstacles, it is now well-accepted that the CNS is r- tinely subject to immune surveillance under both normal as well as diseased con- tions. Indeed, activated cells of the immune system such as T and B lymphocytes and monocyte/macrophages readily infiltrate and accumulate within the CNS f- lowing microbial infection, injury, or upon development of autoimmune responses directed toward resident antigens of the CNS.

Neuroinflammation has been implicated recently in the pathogenesis of many neurodegenerative diseases. The cross-talk between neurons and non-neuronal cells seems to be a critical step in the progression of neurodegeneration and molecules that have a beneficial role may turn into harmful players. Thus, matrix metalloproteinases (MMPs), which are involved in axonal growth and regeneration as well as synaptic plasticity, may also have detrimental effects. Recent evidence has linked MMPs to conditions like ischemia, multiple sclerosis, Alzheimer's disease and suggested that, together with their role in the degradation of extracellular macromolecules, MMPs could work as important signalling molecules from injured neurons to the microglia. Thus, MMP-3 has been shown to induce the release of pro-inflammatory cytokines from microglia via activation of ERK and NF-kB-dependent pathways. Increasing evidence highlights the importance of a balanced cross-talk between neurons and non-neuronal cells and indicates that the presence of reactive astrocytes, the activation of microglia and the release of inflammatory mediators may contribute to the progression of many central nervous system disorders, independently of the nature of the primary pathogenic event. However, many aspects still remain controversial and much more effort is needed to understand the role of neuroinflammatory mediators and processes in these conditions. This volume brings together renowned, international scientists to discuss current knowledge and views on the mechanisms of neuroinflammation, on its role in the context of different neurodegenerative diseases (i.e. Alzheimer's, prion disease, HIV-associated dementia, multiple sclerosis, pain) and on the potential approaches for future therapeutic strategies.

Despite tremendous advances in the understanding of the sensory nervous system which have accompanied the recent explosive growth of the neurosciences, rema- ably few innovative medicines directed towards pain and inflammation are ava- able. Indeed, many patients are still prescribed analgesic and anti-inflammatory medications that were identified long ago as components of herbal remedies. Si- larly, potential new medicines in clinical evaluation based on capsaicin and the c- saicin receptor are both grounded firmly on folk traditions and yet rely upon the most contemporary techniques of drug discovery and delivery. The first formal report of the pain-relieving properties of capsaicin appeared in 1850 [1]. However, for centuries before this, capsaicin-containing extracts had been used as folk medicines in cultures with access to pepper plants, much in the same way as poppy or willow-bark extracts were. Despite widespread use, it was not until 1878 that the selective action of capsaicin on the sensory nervous system was r- ognized [2]. In Chapter 1 of this volume, Janos Szolcsányi reviews this early research, which culminated with the seminal studies of Nicholas Jansco and his c- leagues in Hungary in the 1940s. Since then, capsaicin and related vanilloid c- pounds have played a prominent role in analgesia and inflammation investigations because of their ability to selectively activate a subpopulation of sensory neurons and produce sensations of pain and localized erythema.