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Innate immunity and neurodegenerative disorders

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193103 Year: Pages: 87 DOI: 10.3389/978-2-88919-310-3 Language: English
Publisher: Frontiers Media SA
Subject: Psychiatry --- Therapeutics --- Neurology --- Medicine (General) --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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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.

Neuronal Self-Defense: Compensatory Mechanisms in Neurodegenerative Disorders

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197590 Year: Pages: 190 DOI: 10.3389/978-2-88919-759-0 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Neurodegenerative disorders are characterized by the progressive loss of specific populations of neurons with consequent deterioration of brain's function and dramatic impact on human behavior. At present, there are no effective cures for neurodegenerative diseases. Because unambiguous diagnosis is possible only after manifestation of symptoms, when a large proportion of neurons has been already lost, therapies are necessarily confined to alleviation of symptoms. Development of cures halting the disease course is hampered by our rudimentary understanding of the etiopathology. Most neurodegenerative disorders are sporadic and age-related and - even for those of known genetic origin - the mechanisms influencing disease onset and progression have not been fully characterized. The different diseases, however, share important similarities in the mechanisms responsible for neuronal loss, which is caused by a combination of endogenous and exogenous challenges. Trophic deprivation, oxidative stress, accumulation of abnormal protein aggregates, and bioenergetics defects have been described in most, if not all, neurodegenerative disease. To counterbalance these noxious stimuli cells deploy, at least during the initial pathogenic states, intrinsic neuroprotective responses. These are general compensatory mechanisms, common to several neurodegenerative conditions, which reprogram cellular physiology to overcome stress. Adaptation includes strategies to optimize energetic resources, for instance reduction of rRNA synthesis to repress translation, suppression of transcription, and bioenergetics and metabolic redesign. Additional mechanisms include potentiation of antioxidant capacity, induction of endoplasmic reticulum (ER) stress, and activation of protein quality control systems and autophagy. Ineffective execution of these compensatory strategies severely threatens cellular homeostasis and favors onset of pathology. Therefore, a better understanding of these "buffering" mechanisms and of their interconnections may help to devise more effective therapeutic tools to prolong neuronal survival and activity, independently of the original genetic mutations and stress insults. This Research Topic focuses on the initial compensatory responses protecting against failure of those mechanisms that sustain neuronal survival and activity. The collection intends to summarize the state-of-the-art in this field and to propose novel research contributes, with the ultimate goal of inspiring innovative studies aimed to contrast progression of neurodegenerative diseases.

Berry Antioxidants in Health and Disease

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ISBN: 9783038423485 9783038423492 Year: Pages: VIII, 156 DOI: 10.3390/books978-3-03842-349-2 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Genetics --- Biology
Added to DOAB on : 2017-02-21 07:38:04
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During the last decade, a high volume of work has been published on the health-promoting effects of berries (e.g., blueberries, cranberries, blackberries, etc.) that are rich in antioxidant phytochemicals, polyphenols. Consuming a diet rich in polyphenols has been documented to attenuate the risk of chronic diseases, such as cardiovascular disease, certain cancers, diabetes mellitus, and neurodegenerative disorders. Recent evidence also reveals that the biological effects of polyphenols extend beyond their traditional antioxidant role.This Special Issue includes 10 peer-reviewed papers, including original research papers and reviews. They present the most recent advances in the role of berry antioxidants, not only in maintaining health but also in preventing and/or reversing disease both in cell culture, animal models and in humans. Additionally, the molecular mechanisms and signaling pathways modulated by berry antioxidants are presented. Chapters include the role of berry antioxidants in whole fruit and leaves on the metabolic syndrome, obesity, diabetes and glucose intolerance, cancer, inflammation, oxidative stress and neuroprotection as well as cardiovascular disease. As a guest editor, I would like to acknowledge the authors of all chapters for their valuable contributions and reviewers for their thoughtful and constructive suggestions and time. Special thanks to the publishing team of the Antioxidants Journal for their professionalism, attention to detail and timely completion of this volume.

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