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  • 1
    UID:
    almahu_BV044645660
    Format: xv, 168 Seiten : , Illustrationen.
    Edition: Fifth edition
    ISBN: 978-1-119-16841-6
    Series Statement: At a glance series
    Note: Includes bibliographical references and index
    Additional Edition: Erscheint auch als Online-Ausgabe, PDF ISBN 978-1-119-16843-0
    Language: English
    Subjects: Biology
    RVK:
    Keywords: Neuroanatomie ; Neurophysiologie
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    UID:
    almahu_9948314711202882
    Format: xxi, 314 p. : , ill. (some col.)
    Edition: Electronic reproduction. Ann Arbor, MI : ProQuest, 2015. Available via World Wide Web. Access may be limited to ProQuest affiliated libraries.
    Language: English
    Keywords: Electronic books.
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Online Resource
    Online Resource
    London :Henry Stewart Talks,
    UID:
    edoccha_9961427259102883
    Format: 1 videorecording (40 min., 03 sec.) : , sound, color. , 004003
    Series Statement: Neurodegenerative diseases : fundamentals, research methods, latest advances,
    Content: Audio-visual presentation : Clinical features of HD ; Basic pathogenic mechanisms and pathology ; Current drug therapies ; New disease modifying therapies ; Neural transplants.
    Note: Animated audio-visual presentation with synchronized narration. , Title from title frames. , Updated version of a talk first published in 2007. , Contents: Clinical features of Huntington's Disease -- Basic pathogenic mechanisms and pathology -- Current drug therapies -- New disease modifying therapies -- Neural transplants.
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    Online Resource
    Online Resource
    Frontiers Media SA | [Lausanne, Switzerland] :Frontiers Media SA,
    UID:
    edoccha_9958116393202883
    Format: 1 online resource (87 pages) : , illustrations; digital, PDF file(s).
    ISBN: 9782889193103 (ebook)
    Series Statement: Frontiers Research Topics
    Content: 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 involving 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 long-term 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.
    Note: English
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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  • 5
    Online Resource
    Online Resource
    Frontiers Media SA | [Lausanne, Switzerland] :Frontiers Media SA,
    UID:
    almahu_9947382120502882
    Format: 1 online resource (87 pages) : , illustrations; digital, PDF file(s).
    ISBN: 9782889193103 (ebook)
    Series Statement: Frontiers Research Topics
    Content: 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 involving 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 long-term 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.
    Note: English
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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  • 6
    Online Resource
    Online Resource
    Frontiers Media SA | [Lausanne, Switzerland] :Frontiers Media SA,
    UID:
    edocfu_9958116393202883
    Format: 1 online resource (87 pages) : , illustrations; digital, PDF file(s).
    ISBN: 9782889193103 (ebook)
    Series Statement: Frontiers Research Topics
    Content: 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 involving 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 long-term 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.
    Note: English
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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  • 7
    Online Resource
    Online Resource
    New York :Oxford University Press,
    UID:
    edocfu_9959233301902883
    Format: 1 online resource (337 p.)
    Edition: 1st ed.
    ISBN: 0-19-020873-2 , 0-19-934900-2 , 1-282-76325-3 , 9786612763250 , 0-19-970788-X
    Content: Parkinson's disease becomes apparent only after substantial loss (〉60%) of the dopamine neurons in the substantia nigra. By this time there has already been widespread neural inclusion formation in the peripheral and central nervous system of patients with the disease, although this has only been recognized more recently. Degeneration in these widespread regions of the peripheral and central nervous system is now known to impact on disease symptoms, progression and treatment over time. This book aims to provide a comprehensive review of these non-dopamine lesions in Parkinson's disease by asse
    Note: Description based upon print version of record. , Contents; Contributors; Chapter 1: Lesions Associated with the Classic Triad of Parkinsonian Motor Features; Chapter 2: Lesions Associated with Motor Speech; Chapter 3: Lesions Associated with Eye Movements; Chapter 4: Olfactory Dysfunction in Parkinson's Disease and Related Disorders; Chapter 5: Lesions Associated with Autonomic Dysfunction A: Swallowing Disorders and Drooling; Chapter 6: Lesions Associated with Pain and Sensory Abnormalities; Chapter 7: Lesions Associated with Sleep Disturbances; Chapter 8: Lesions Associated with Depression and Apathy , Chapter 9: Lesions Associated with Dyskinesias and the Dopamine Dysregulation SyndromeChapter 10: Lesions Associated with Visual Hallucinations and Psychoses; Chapter 11: Lesions Associated with Cognitive Impairment and Dementia; Chapter 12: Systemic Manifestations of Parkinson's Disease; Index , English
    Additional Edition: ISBN 0-19-537108-9
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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