Migraine A Neuroinflammatory Disease

The potential involvement of neurogenic inflammation in the pathogenesis of the migraine headache and the inhibition of this mechanism as a possible mode of action of antimigraine medications are discussed in great depth in this volume. The topics are approached from a pathophysiological as well as a clinical experimental perspective by a renowned group of clinicians and scientists who carefully consider the current, future, and potential therapeutic approaches to migraine treatment. The first chapters of the book address the impact of migraine on a personal and societal level, the presentation, pathogenesis and treatment of migraine as well as the role of neurogenic inflammation. Subsequent chapters present models of neurogenic inflammation related to the pathogenesis of the migraine headache, focussing on the mediators and their receptors, as well as on the involvement of mast cells. The possibility of inhibition of neurogenic inflammation in abortive and preventive migraine treatment is also extensively discussed and a chapter on the question of whether migraine is a neuroinflammatory disease concludes this comprehensive analysis. Clinicians and scientists interested in inflammation from a physiological or pharmacological perspective and those interested in the pathogenesis of headache - migraine in particular - are the intended audience for this unique body of work.

Research into inflammatory mechanisms that may cause damage to the Alzheimer's disease (AD) brain has now been ongoing for nearly two decades. Some two dozen clinical studies have strongly suggested that conventional anti-inflammatory drugs may be useful to delay the onset or slow the progression of the disorder. Moreover, virtually all the major systems of the innate immune response appear to be present, and most are upregulated, in pathologically-vulnerable regions of the AD brain. These new findings are described in this volume - first in overview form, followed by chapters on topics of special interest. In many ways, to understand AD brain inflammation, one need only review a text on peripheral inflammation biology, leaving out the chapters on humoral medi ators and substituting microglia for macrophages. In several other key respects, however, AD brain inflammation is unique, due primarily to idiosyncratic interac tions of inflammatory mediators and mechanisms with classical AD pathology: amyloid ~ peptide(A~) deposits and neurofibrillary tangles (NFTs). For this reason, some key concepts about the inflammation that occurs in AD may warrant discus sion in preparation for the more detailed chapters that follow.

In its different presentations, headache is one of the most commonsymptoms seen by family practitioners. The difficulty is indiagnosing the cause of the headache so that the appropriatetreatment is provided, or if referral to a specialist is therecommended course of action. The ABC of Headache helps with this dilemma and guidesthe healthcare professional to look for the possible causes ofpresenting symptoms. Based on real case histories, each chapterguides the reader from symptoms through to diagnosis andmanagement. This new ABC is a highly illustrated, informative, andpractical source of knowledge. With links to further informationand resources, it is a valuable text for healthcare professionalsat all levels of practice and training.

The Molecular Immunology of Neurological Diseases provides a comprehensive review of current updates in molecular immunogenetics of different neurological diseases. Readers will learn about the role of immune cells and their modulation strategies to help in the development of therapeutic approaches for both acute and chronic neurodegenerative disorders. There is no other book available on the topic. It has long been thought that the brain is an immune-privilege organ with very limited immune response. However recent studies have made clear that both systemic 'brain' and peripheral 'blood' immune cell responses play key roles in determining brain pathology in neurodegenerative disorders. This book summarizes the role of immune cell activation in the central nervous system microenvironment in acute and chronic neurodegenerative disorders. In addition, it discusses the key role of immune cells and their modulation strategies for the development of current therapeutic approaches. Discusses the molecular immunogenetics of different neurological diseases Covers strategies for the development of therapeutic approaches Encompasses both acute and chronic neurogenerative disorders Describes the molecular pathogenesis of viral genes in various diseases Features chapters on migraine, muscular dystrophy and cancer

This book deals with the description of the role of chemokines in immune response and underlines potential targets of therapeutical intervention. It offers a series of international contributions of the most challenging aspects of lymphocyte migration in homeostasis and in disease, and has a special focus on diseases and targets of therapeutical intervention. The book will interest researchers and clinicians from inflammation research.

The understanding how complement relates to glomerular diseases has evolved considerably during the last years. Substantial evidence has accumulated that explain how a defective or deregulated complement system results in kidney diseases. The combination and close interaction of basic research with clinical medicine has demonstrated an important role of complement effector and regulatory proteins in pathological settings of the kidney. A large panel of distinct human kidney diseases such as hemolytic uremic syndrome (HUS), membrano proliferative glomerulonephritis (MPGN), systemic lupus erythematosus (SLE) and in ischemic reperfusions injury and transplantation are caused by defective complement control. Genetic analyses have identified mutations in complement regulators that are associated with these diseases. Mutations have been identified in the fluid phase alternative pathway regulator Factor H and the membrane regulator Membrane Cofactor Protein MCP (CD46). The functional characterization of the mutant proteins allows to define the pathophysiological events on a molecular level. These new concepts and data on disease mechanisms already allowed to establish new diagnostic and novel promising therapeutic approaches for several human kidney diseases.

Rheumatoid Arthritis (RA) represents a complex disease where the inheritable component has been estimated to be up to 60%. This PIR volume deals with the genetic basis and regulation of rheumatic diseases. The first part of the book describes genetic studies on rheumatic diseases. The second part deals with the shared heredity of rheumatic diseases, e.g., RA, lupus and ankylosing spondylitis. The third part of the volume describes tools for analysing genetic complexity, ranging from animal models to new molecular tools. The volume is essential reading for researchers and clinicians from rheumatology, inflammation research, immunology, and cell and molecular biology.