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Author : Maya Koronyo-Hamaoui,Sally Ann Frautschy,Jorge Ivan Alvarez
Publisher : Frontiers Media SA
Page : 461 pages
File Size : 45,6 Mb
Release : 2022-07-13
Category : Medical
ISBN : 9782889765621
Author : Grzegorz Kreiner,Andrii Domanskyi,Małgorzata Kujawska
Publisher : Frontiers Media SA
Page : 280 pages
File Size : 50,5 Mb
Release : 2021-11-01
Category : Science
ISBN : 9782889715633
Author : Valerie Sackmann
Publisher : Linköping University Electronic Press
Page : 60 pages
File Size : 44,9 Mb
Release : 2019-10-16
Category : Electronic
ISBN : 9789175190129
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 : M. A. Yenari,Rona Greenberg Giffard
Publisher : Nova Science Publishers
Page : 290 pages
File Size : 50,5 Mb
Release : 2006
Category : Medical
ISBN : UVA:X030116408
The brain has long been considered an immune privileged organ, meaning that inflammatory cells are excluded due to a relatively impenetrable blood brain barrier (BBB). However, this is not to say that the central nervous system is incapable of eliciting immune responses, as resident inflammatory cells exist within the brain parenchyma. Microglia have long been thought to be the brain's resident immune cell with myeloid lineage similar to monocytes and macrophages. In this volume, the authors review the current state of knowledge with regard to immune responses and cell-cell interactions as they pertain to a variety of neurodegenerative diseases. The changing role of inflammation with development is considered. They also present a summary of the various therapeutic strategies employed both in the laboratory and at the clinical level.
Author : Phillip K. Peterson,Michal Toborek
Publisher : Springer
Page : 606 pages
File Size : 43,6 Mb
Release : 2014-07-08
Category : Medical
ISBN : 9781493910717
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.
Author : Francesca Gilli,Roberta Magliozzi,Laura Piccio,Enrique Alvarez
Publisher : Frontiers Media SA
Page : 132 pages
File Size : 55,7 Mb
Release : 2021-11-15
Category : Medical
ISBN : 9782889716388
Author : Peter Riederer,Heinz Reichmann,Moussa B. H. Youdim,Manfred Gerlach
Publisher : Springer Science & Business Media
Page : 484 pages
File Size : 51,8 Mb
Release : 2006-11-23
Category : Medical
ISBN : 9783211452950
This book gives a comprehensive overview on current clinical and basic research issues related to Parkinson’s disease and its related disorders. The book is the result of the 16th International Congress of Parkinson’s Disease and Related disorders congress 2005. Its contents are suitable for neurologists, psychiatrists, neurosurgeons, basic researchers, geneticians and patients as well as their relatives.
Author : Paul L. Wood
Publisher : Springer Science & Business Media
Page : 411 pages
File Size : 46,5 Mb
Release : 2002-12-18
Category : Medical
ISBN : 9781592592975
In this thoroughly updated and revised edition of his much praised book, Paul L. Wood and a panel of leading researchers capture these new developments in a masterful synthesis of what is known today about the inflammatory mediators and cells involved in neurodegenerative diseases. This second edition contains extensive updates on the mediators produced by microglia and their role in neuroinflammatory-induced neuronal lysis. There is also increased coverage of the animal models used in the study of neuroinflammatory mechanisms, of the new imaging methods that allow the noninvasive evaluation of microglial activation in human neurodegernerative disorders, and of the role of neuroinflammation in amyloid-dependent neuronal lysis.
Author : Deng-Feng Zhang,Gjumrakch Aliev,Feiqi Zhu,Xian-Le Bu
Publisher : Frontiers Media SA
Page : 153 pages
File Size : 42,6 Mb
Release : 2021-10-25
Category : Science
ISBN : 9782889715435
Author : Fei Yin,Jia Yao,Roberta Diaz Brinton,Enrique Cadenas
Publisher : Frontiers Media SA
Page : 161 pages
File Size : 55,6 Mb
Release : 2017-08-16
Category : Electronic book
ISBN : 9782889452538
Impairment of energy metabolism is a hallmark of brain aging and several neurodegenerative diseases, such as the Alzheimer’s disease (AD). Age- and disease-related hypometabolism is commonly associated with oxidative stress and they are both regarded as major contributors to the decline in synaptic plasticity and cognition. Neuroinflammatory changes, entailing microglial activation and elevated expression of inflammatory cytokines, also correlate with age-related cognitive decline. It is still under debate whether the mitochondrial dysfunction-induced metabolic deficits or the microglia activation-mediated neuroinflammation is the initiator of the cognitive changes in aging and AD. Nevertheless, multiple lines of evidence support the notion that mitochondrial dysfunction and chronic inflammation exacerbate each other, and these mechanistic diversities have cellular redox dysregulation as a common denominator. This research topic focuses on the role of a metabolic-inflammatory axis encompassing the bioenergetic activity, brain inflammatory responses and their redox regulation in healthy brain aging and neurodegenerative diseases. Dynamic interactions among these systems are reviewed in terms of their causative or in-tandem occurrence and how the systemic environment, –e.g., insulin resistance, diabetes, and systemic inflammation–, impacts on brain function.
Author : Morena Zusso,Stefano Moro,Pietro Giusti,Leanne Stokes
Publisher : Frontiers Media SA
Page : 282 pages
File Size : 40,6 Mb
Release : 2020-07-14
Category : Electronic
ISBN : 9782889638543
Author : Stephen C. Bondy,Arezoo Campbell
Publisher : Springer
Page : 405 pages
File Size : 48,9 Mb
Release : 2016-12-14
Category : Science
ISBN : 9783319334868
The book describes the major degenerative processes and pathologies exacerbated by senescence and how they can be alleviated through retardation of cellular aging. Topics discussed include neurodegenerative disease, protein oxidation, cerebrovascular disease, particle-induced inflammation and cardiovascular disease, Alzheimer’s disease, ovarian aging, dietary and endogenous anti-oxidants in management of Parkinson’s disease, and effects of exercise on oxidation and inflammation. The nineteen expertly authored chapters are organized into three sections in order to present a complete picture to the reader: Age Related Cellular Events, Role of Inflammatory and Oxidative Processes in Age-Related Diseases, and Retardation of Cellular Aging. Inflammation, Oxidative Stress and Age-Related Disease draws from a variety of international perspectives and provides a comprehensive overview of the relationship between disease, cell aging, and oxidative stress, as well as potential for preventing or slowing these processes. This installment of Springer’s Oxidative Stress in Applied Basic Research and Clinical Practice is ideal for researchers, clinicians, and advanced graduate students in the fields of cardiology, neuroscience, biogerontolgy, and cell biology.
Author : Nicola Woodroofe,Sandra Amor
Publisher : John Wiley & Sons
Page : 462 pages
File Size : 53,7 Mb
Release : 2014-04-15
Category : Medical
ISBN : 9781118406540
The last decade has seen an upsurge of information on the role of immune responses in neurodegenerative disorders. In many of these diseases it is still unclear whether the innate and adaptive responses are pathogenic or play a role in repair, and thus understanding their precise roles is key to controlling these diseases by designing immune-therapeutic approaches. The connection between many neurological diseases is the realisation that the immune and nervous systems are inextricable linked, and that perturbations in this delicate balance are involved in many disorders. This has opened up new avenues for therapeutic approaches to treatment of CNS inflammatory and neurodegenerative disorders. Neuroinflammation and CNS Disorders brings together the very latest information on the interactions between the immune system and central nervous system. The first section of the book highlights the basic concepts in the field whilst the second section, the main body of the book, covers the role of the immune response in specific disorders of the central nervous system. Neuroinflammation and CNS Disorders will provide an invaluable guide for both researchers and clinicians working in this complex and dynamic field.
Author : Anonim
Publisher : Academic Press
Page : 352 pages
File Size : 42,8 Mb
Release : 2019-02-15
Category : Science
ISBN : 9780128157176
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
Author : Giacinto Bagetta,Stuart Lipton,M. Tiziana Corasaniti
Publisher : Elsevier
Page : 499 pages
File Size : 48,9 Mb
Release : 2007-07-25
Category : Medical
ISBN : 9780080550565
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.