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Author: J. Miklossy
Publisher: IOS Press
ISBN: 1614997063
Category : Medical
Languages : en
Pages : 420
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Book Description
Alzheimer’s disease is one of the biggest emerging public health problems in the world. Although the last four decades have yielded important insights into the pathogenesis of Alzheimer’s disease, its cause is still unclear, and if it is not discovered the world will face an unprecedented healthcare problem by the middle of this century. In recent years, evidence of the microbial origin of various chronic inflammatory disorders – including several neurodegenerative, neuropsychiatric and other systemic disorders – has been steadily growing. Accumulating new and historic observations are providing evidence of an association between Alzheimer’s disease and certain infectious agents, and may offer new opportunities for ground-breaking healthcare solutions. This handbook assembles and connects findings with regard to the infectious origin of Alzheimer’s disease, and the data presented in its chapters deserves the attention of the neuroscience community, physicians and the health departments of governments worldwide by virtue of its amount and quality. This handbook offers a comprehensive overview of the current knowledge regarding the topic of infection and Alzheimer’s disease, which could pinpoint the cause of this disease. Influential diagnosis, treatment and prevention strategies may also emerge from this crucial research area.
Author: J. Miklossy
Publisher: IOS Press
ISBN: 1614997063
Category : Medical
Languages : en
Pages : 420
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Book Description
Alzheimer’s disease is one of the biggest emerging public health problems in the world. Although the last four decades have yielded important insights into the pathogenesis of Alzheimer’s disease, its cause is still unclear, and if it is not discovered the world will face an unprecedented healthcare problem by the middle of this century. In recent years, evidence of the microbial origin of various chronic inflammatory disorders – including several neurodegenerative, neuropsychiatric and other systemic disorders – has been steadily growing. Accumulating new and historic observations are providing evidence of an association between Alzheimer’s disease and certain infectious agents, and may offer new opportunities for ground-breaking healthcare solutions. This handbook assembles and connects findings with regard to the infectious origin of Alzheimer’s disease, and the data presented in its chapters deserves the attention of the neuroscience community, physicians and the health departments of governments worldwide by virtue of its amount and quality. This handbook offers a comprehensive overview of the current knowledge regarding the topic of infection and Alzheimer’s disease, which could pinpoint the cause of this disease. Influential diagnosis, treatment and prevention strategies may also emerge from this crucial research area.
Author: Roger A Barker
Publisher: Frontiers E-books
ISBN: 2889193101
Category : Medicine (General)
Languages : en
Pages : 88
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Book Description
Inflammation of the brain in the context of neurodegenerative disorders is an area of intense debate and discussion, not least in terms of its pathogenic significance and the extent to which it drives disease processes and pathology. This inflammation can take several forms including innate responses recruiting microglia, humoral responses involving antibody, complement mediated processes and cellular T-cell activation, of which the role and extent of each may differ between diseases. Whilst some diseases have been more intensely linked to inflammation and long-term degeneration (e.g. MS), more traditional chronic neurodegenerative disorders have been thought of in terms of intrinsic neuronal pathology with a secondary innate response. However, it has been described that microglia activation is an early event of many degenerative disorders and evidence is accumulating that it may play a critical role in actually causing pathology and driving disease processes. If true, this would have major therapeutic implications, but what is the evidence that this is the case? The initial observations by Patrick McGeer’s group of post-mortem tissue from patients with Parkinson’s disease revealed the presence of activated brain microglia and has thus lead to the hypothesis that chronic inflammation could participate to neuronal degenerative processes. The significance of these original observations has only been recently revisited, and the development of more powerful tools to study the brain immune response has certainly contributed to this field of research. Chronic inflammation in the brain can take many forms but of particular interest has been the resident microglia and the role they play in this process. In this context, microglia have often been thought to become activated only after the disease has begun and then to contribute minimally to the degenerative process. Emerging new concepts challenge this view by proposing that microglial senescence, for example, may release the disease process and/or accelerate it. In addition, microglia, once activated, can adopt different phenotypes which can be both pro-inflammatory and pro-repair and may impact not only on the healthy adult neuronal population but on those new neurons derived from neurogenic niches of the adult brain. In this Research Topic, we attempt to explore this by first considering the innate immune responses in the brain and the methods by which they can be studied experimentally and in patients with various neurodegenerative disorders. This sets the scene for then discussing a range of different disorders including Alzheimer’s, Parkinson’s, Huntington’s disease and amyotrophic lateral sclerosis. These papers seek to discuss the evidence for an innate immune response and whether this is beneficial or detrimental, as well as its therapeutic implications.
Author: Uday Kishore
Publisher: BoD – Books on Demand
ISBN: 9535110888
Category : Medical
Languages : en
Pages : 642
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Book Description
This book highlights the pathophysiological complexities of the mechanisms and factors that are likely to be involved in a range of neuroinflammatory and neurodegenerative diseases including Alzheimer's disease, other Dementia, Parkinson Diseases and Multiple Sclerosis. The spectrum of diverse factors involved in neurodegeneration, such as protein aggregation, oxidative stress, caspases and secretase, regulators, cholesterol, zinc, microglia, astrocytes, oligodendrocytes, etc, have been discussed in the context of disease progression. In addition, novel approaches to therapeutic interventions have also been presented. It is hoped that students, scientists and clinicians shall find this very informative book immensely useful and thought-provoking.
Author: Shailendra K. Saxena
Publisher: BoD – Books on Demand
ISBN: 1838807659
Category : Medical
Languages : en
Pages : 416
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Book Description
The book focuses on various aspects and properties of innate immunity, whose deep understanding is integral for safeguarding the human race from further loss of resources and economies due to innate immune response-mediated diseases. Throughout this book, we examine the individual mechanisms by which the innate immune response acts to protect the host from pathogenic infectious agents and other non-communicable diseases. Written by experts in the field, the volume discusses the significance of macrophages in infectious disease, tumor metabolism, and muscular disorders. Chapters cover such topics as the fate of differentiated macrophages and the molecular pathways that are important for the pathologic role of macrophages.
Author: Robert R. Rich
Publisher: Mosby Incorporated
ISBN: 9780323044042
Category : Medical
Languages : en
Pages : 1578
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Book Description
Offers answers to challenges in clinical immunology. This book contains immunology knowledge and includes a companion web site to give you two ways to find the answers you need.
Author: Valerie Sackmann
Publisher: Linköping University Electronic Press
ISBN: 9175190125
Category :
Languages : en
Pages : 69
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Book Description
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative diseases with rates increasing along with the ageing global population. Despite best efforts, we still do not understand the etiopathogenesis of these diseases and there are no effective disease-modifying treatments. Cognitive deficiencies or motor complications that emerge during AD and PD are thought to be the result of the accumulation of misfolded, aggregate-prone proteins, such as amyloid-? (A?) and tau or ?-synuclein (?-syn), respectively. Growing evidence suggests that prefibrillar oligomers of A? and ?-syn (oA? and o?-syn) are key contributors to the progression of these diseases. The progressive accumulation of these proteins leads to a gradual spread of pathology throughout interconnected brain regions, but the mechanisms by which this spreading occurs are still largely unknown. Neuroinflammation has been recognised as an important contributor to neurodegenerative disease. It is hypothesised that a pro-inflammatory environment initiated by the innate immune system, either through activation from A? itself or indirectly through neuronal injury signals in AD. These phenomena are thought to either cause or accelerate AD, such that an anti-inflammatory approach may be neuroprotective. In paper I, we investigated whether different inflammatory environments affected the transfer of oA? between neuron-like cells, in addition to investigating inter- and intracellular protein changes. This study demonstrated that an anti-inflammatory environment reduces the transfer of oA? between cells. We also provide evidence that these cells begin to take on the “phenotype” of the inflammatory milieu, while also demonstrating that the expression profile of endosomal/lysosomal and protein trafficking proteins is altered during these conditions. Small extracellular vesicles called exosomes, which are key players in cell to cell communication, have been proposed to play an influential role in spreading neurodegenerative proteins between cells. Exosomes are small membranous vesicles that are formed by the inward budding of multivesicular bodies (MVBs). These MVBs can then merge with the plasma membrane to be released into the extracellular environment as vesicles, which serve as vehicles for transferring proteins, lipids, and mRNAs between cells. The ESCRT-dependent pathway is the most understood mechanism underlying exosome biogenesis. However, exosomes can also be formed through ESCRT-independent pathways, including through the hydrolysis of sphingomyelin by neutral sphingomyelinase 2 (nSMase2), which produces ceramide. Paper II investigated whether exosomes formed through an ESCRT-independent pathway plays a significant role in the transfer of o?-syn between neuron-like cells. As oxidative stress is a common feature in PD brains, which in turn dysregulates nSMase2 activity, we also tested our model under hypoxic conditions. Inhibition of nSMase2 significantly reduced the transfer of o?-syn between cells but also resulted in decreased ?-syn aggregation. Hypoxia did not influence o?-syn transfer, however, it significantly dysregulated the sphingolipid composition, which may be important for ?-syn binding to exosomes and exosome communication. During AD and PD, there is a noted reduction in the effectiveness of autophagy, a process critical to cellular proteostasis. Recent studies have uncovered shared regulatory mechanisms of exosome biogenesis and autophagy, suggesting that they are closely linked. Previous findings have shown that inhibition of autophagy in AD mice mediates A? trafficking through altering the secretion of A? in MVBs. To further study this effect, we investigated the interplay between autophagy and exosome secretion using ATG7 knock-out x APPNL-F knock-in AD mice in paper III. These autophagy-deficient AD mice had a reduced extracellular A? plaque load, but increased intracellular A?, which was found to be assembled into higher-ordered assemblies. While exosomal secretion was dysregulated in these mice, the amount of A? packaged into the exosomes was unchanged. Lastly, one of the biggest challenges in developing effective treatments for AD is the lack of early diagnosis of living patients. As the connection between exosomes and the spread of neurodegenerative proteins is still relatively new, there remains a diagnostic potential to be explored with exosomes. Paper IV aimed to develop a new diagnostic assay to detect oA? in exosomes isolated from human cerebrospinal fluid. Although exosomal oA? was readily detected in some of these samples, the assay’s sensitivity requires additional optimisation before it can be further validated for the clinic. In summary, the studies presented in this thesis have furthered our understanding of how inflammation, autophagy, and exosomes contribute to the intercellular transmission of AD and PD associated proteins. We have shown that an anti-inflammatory approach may slow down the progression of AD through reducing the transfer of oA? between cells. We also provide novel findings relating to the biogenesis of exosomes, which in turn affected the ability of exosomes to transmit neurodegenerative proteins between cells, and their association with autophagic processes. Finally, we have investigated the feasibility of exosomes as an early AD diagnostic marker. This work has helped to elucidate some of the mechanisms underlying the progression of neurodegenerative diseases, which may be useful targets for the investigation of new therapeutic avenues.
Author: A.D. Roses
Publisher: Springer Science & Business Media
ISBN: 3642801099
Category : Medical
Languages : en
Pages : 208
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Book Description
There is now considerable genetic evidence that the type 4 allele of the apolipoprotein E gene is a major susceptibility factor associated with late-onset Alzheimer's disease, the common form of the disease defined as starting after sixty years of age. The role of apolipoprotein E in normal brain metabolism and in the pathogenesis of Alzheimer's disease are new and exciting avenues of research. This book, written by the most outstanding scientists in this new filed, is the first presentation of results concerning the implications of apolipoprotein E on the genetics, cell biology, neuropathology, biochemistry, and therapeutic management of Alzheimer's disease.
Author: Golam Khandaker
Publisher: Cambridge University Press
ISBN: 1009038362
Category : Medical
Languages : en
Pages : 357
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Book Description
The rapidly growing field of immunopsychiatry combines expertise and insights from immunology, psychiatry and neuroscience to understand the role of inflammation and other immune processes in causing and treating mental illness. This represents a major shift in mental health science, traditionally focused on psychological and neuronal mechanisms of depression, psychosis and dementia. This book provides the first comprehensive overview of recent, inter-disciplinary research linking disordered function of the immune system to the brain and mental illness. It offers a broad and deep perspective on the implications of immune system involvement in psychiatric disorders, including a balanced focus on basic science and clinical applications. Chapters cover the scientific evidence linking immune processes to major mental illnesses such as schizophrenia, depression, anxiety and dementia. An invaluable guide for graduate students, doctors in training, scientific researchers and others interested in the link between the immune system and mental health.
Author: Tsuneya Ikezu
Publisher: Springer
ISBN: 3319440225
Category : Medical
Languages : en
Pages : 1045
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Book Description
The second edition of Neuroimmune Pharmacology bridges the disciplines of neuroscience, immunology and pharmacology from the molecular to clinical levels with particular thought made to engage new research directives and clinical modalities. Bringing together the foremost field authorities from around the world, Neuroimmune Pharmacology will serve as an invaluable resource for the basic and applied scientists of the current decade and beyond.
Author: Cary L. Cooper
Publisher: Ediciones Díaz de Santos
ISBN: 9780471904779
Category : Health & Fitness
Languages : en
Pages : 348
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Book Description
Psychosocial Stress and Cancer Edited by Cary L. Cooper University of Manchester Institute of Science and Technology The importance of stress in the development of heart disease is well established, but its role in cancer is only just beginning to be investigated. Recent research in humans indicates that various life events, personality pre-dispositions, as well as immunological and central nervous system interactions, may trigger the cancer process, or at the very least accentuate its development. In this book, a number of recognized international authorities provide state-of-the-art statements on the key issues of the subject. Beginning with a review of the findings to date, there follows more in-depth analysis of potential social/psychological precursors to cancer, and the way in which they may influence the aetiology and development of the disease. The final section deals with the way in which psychosocial factors may be managed in cancer patients, and provides a comparative summary of the various methodological approaches utilized in studies exploring the field of psychological oncology. The book will provide a unique digest of current knowledge as well as a starting point for future research, and will be invaluable to all concerned with the study and management of the cancer process. Other Wiley titles on this subject include: Stress Research: Issues for the Eighties Edited by Cary L. Cooper 160 pages February 1983 Mind and Cancer Prognosis Basil A. Stoll, St Thomas’s Hospital and Royal Free Hospital, London 214 pages December 1979 All about Cancer Chris Williams, CRC Medical Oncology Unit, University of Southampton 404 pages April 1983
