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Author : Grzegorz Kreiner,Andrii Domanskyi,Małgorzata Kujawska
Publisher : Frontiers Media SA
Page : 280 pages
File Size : 42,7 Mb
Release : 2021-11-01
Category : Science
ISBN : 9782889715633
Author : Valerie Sackmann
Publisher : Linköping University Electronic Press
Page : 60 pages
File Size : 47,8 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 : Maya Koronyo-Hamaoui,Sally Ann Frautschy,Jorge Ivan Alvarez
Publisher : Frontiers Media SA
Page : 461 pages
File Size : 40,8 Mb
Release : 2022-07-13
Category : Medical
ISBN : 9782889765621
Author : Anonim
Publisher : Elsevier Health Sciences
Page : 1578 pages
File Size : 41,5 Mb
Release : 2008
Category : Clinical immunology
ISBN : 0323044042
Author : Jonas H. Ellenberg,William C. Koller,James William Langston
Publisher : CRC Press
Page : 600 pages
File Size : 45,5 Mb
Release : 1995-03-01
Category : Medical
ISBN : 0824788230
This comprehensive reference provides a detailed overview of current concepts regarding the cause of Parkinson's disease-emphasizing the issues involved in the design, implementation, and analysis of epidemiological studies of parkinsonism.
Author : Rosa Barrio,James D. Sutherland,Manuel S. Rodriguez
Publisher : Springer Nature
Page : 350 pages
File Size : 40,8 Mb
Release : 2020-04-09
Category : Science
ISBN : 9783030382667
This book, written by members of the European network PROTEOSTASIS, provides an up-to-date review of the research regarding protein homeostasis in health and disease. With new discoveries contributing to the increasing complexity of this topic, the book offers a detailed overview of the pathways regulating protein homeostasis, including autophagy and the ubiquitin protein family. Following a basic introduction, it explains how defects in protein homeostasis contribute to numerous pathologies, including cancer, neurodegeneration, inflammation and a number of rare diseases. In addition, it discusses, the role of protein homeostasis in cellular development and physiology. Highlighting the latest research in the field of protein homeostasis and its implications for various clinically relevant diseases, the book appeals to researchers and clinicians, while also offering a reference guide for scholars who are new to the field.
Author : G. Ali Qureshi,S. Hasan Parvez
Publisher : Elsevier
Page : 794 pages
File Size : 48,9 Mb
Release : 2007-03-22
Category : Science
ISBN : 0080489494
Oxidative stress is the result of an imbalance in pro-oxidant/antioxidant homeostasis that leads to the generation of toxic reactive oxygen species. Brain cells are continuously exposed to reactive oxygen species generated by oxidative metabolism, and in certain pathological conditions defense mechanisms against oxygen radicals may be weakened and/or overwhelmed. DNA is a potential target for oxidative damage, and genomic damage can contribute to neuropathogenesis. It is important therefore to identify tools for the quantitative analysis of DNA damage in models on neurological disorders. This book presents detailed information on various neurodegenerative disorders and their connection with oxidative stress. This information will provide clinicians with directions to treat these disorders with appropriate therapy and is also of vital importance for the drug industries for the design of new drugs for treatment of degenerative disorders. * Contains the latest information on the subject of neurodegenerative disorders * Reflects on various factors involved in degeneration and gives suggestions for how to tackle these problems
Author : Bijo Mathew,Della Grace Thomas Parambi
Publisher : Springer Nature
Page : 198 pages
File Size : 50,5 Mb
Release : 2020-09-21
Category : Medical
ISBN : 9789811551673
This book provides medical professionals and researchers with a comprehensive overview of fundamental concepts and recent advances in neurochemistry, and offers new perspectives for all those involved with research in related disciplines. As drug discovery for neurodegenerative diseases is one of the largest subspecialties in the field of medicine, the book addresses topics that transcend the borders between disciplines, and presents a wealth of investigations into and discussions on critical questions relevant to the entire field of CNS drug research. It summarizes the available data on the fundamentals of neurotransmitters, treatment of and advanced care for neurodegenerative diseases; and outlines current and future research directions in this field. Combining both conventional and innovative approaches to the topic, the book offers a valuable guide for readers working in medicinal chemistry, the life sciences and allied fields.
Author : Valquiria Bueno,Graham Pawelec
Publisher : Springer Nature
Page : 208 pages
File Size : 47,8 Mb
Release : 2021-11-10
Category : Medical
ISBN : 9783030875329
This book presents studies of the main conditions that affect health and well-being of old people. Considering the present scenario of COVID-19, the effects of this viral infection on individuals older than 65 years are also discussed. The content enables professionals of health and government for the present and future actions in this important area. Readers go through the changes occurring in organs and tissues that can interfere with susceptibility to infections, low response to vaccines, cancer, and loss of cognition during the aging process. A discussion of the central role played by the immune system in the age-related diseases and how the immunity can be impaired during the ageing process is presented. Possibilities to circumvent these conditions via healthy habits in diet, physical exercise, and new pharmacological interventions are part of the content. This book discusses how human healthy longevity is dependent, at least in part, of a functional immune system. Chapters were written for researchers in the field of aging and is especially suited for those interested in the study of immunosenescence and inflammaging affecting the health of old individuals.
Author : Michael S. Wolfe
Publisher : Academic Press
Page : 560 pages
File Size : 41,6 Mb
Release : 2018-03-29
Category : Medical
ISBN : 9780128113059
The Molecular and Cellular Basis of Neurodegenerative Diseases: Underlying Mechanisms presents the pathology, genetics, biochemistry and cell biology of the major human neurodegenerative diseases, including Alzheimer’s, Parkinson’s, frontotemporal dementia, ALS, Huntington’s, and prion diseases. Edited and authored by internationally recognized leaders in the field, the book's chapters explore their pathogenic commonalities and differences, also including discussions of animal models and prospects for therapeutics. Diseases are presented first, with common mechanisms later. Individual chapters discuss each major neurodegenerative disease, integrating this information to offer multiple molecular and cellular mechanisms that diseases may have in common. This book provides readers with a timely update on this rapidly advancing area of investigation, presenting an invaluable resource for researchers in the field. Covers the spectrum of neurodegenerative diseases and their complex genetic, pathological, biochemical and cellular features Focuses on leading hypotheses regarding the biochemical and cellular dysfunctions that cause neurodegeneration Details features, advantages and limitations of animal models, as well as prospects for therapeutic development Authored by internationally recognized leaders in the field Includes illustrations that help clarify and consolidate complex concepts
Author : Ralph N. Martins,Charles S. Brennan,Binosha Fernando,Margaret A. Brennan,Stephanie J. Fuller
Publisher : John Wiley & Sons
Page : 548 pages
File Size : 43,8 Mb
Release : 2019-07-10
Category : Technology & Engineering
ISBN : 9781119356783
Understanding the impact of diet, exercise, genetics, and hormones on the risk and development of Alzheimer’s and other neurogenerative diseases Diet is widely known to impact on neurological function. Nevertheless, academic texts discussing this relationship are relatively few in number. This book therefore fills an important gap in the current literature. Opening with an overview of neurodegenerative diseases, particularly Alzheimer’s disease, the text then focuses on explaining the means by which glycemic control and lipid metabolism – and associated nutritional and lifestyle variables – may factor into such disorders’ prevention and treatment. An international group of experts in the fields of food science and neurodegeneration have contributed chapters that examine Alzheimer’s disease within a broad range of contexts. Offering dietary, genetic, and hormonal perspectives, the authors explore topics ranging from sugar consumption to digestive fermentation, and Alzheimer’s disease animal models to the cognition-enhancing effects of physical exercise. Also included are overviews of the latest research into current and developing methods of treatment and diagnosis, as well as differential diagnostics. This groundbreaking book: Explores how glucose metabolism, insulin resistance, lipid metabolism, and high intake of refined carbohydrates are linked to Alzheimer's disease Discusses how genetic makeup can impact risk of Alzheimer’s and Parkinson’s disease Examines cognitive changes in neurodegeneration, lists current tests for determining cognitive impairment, and provides information concerning differential diagnosis Discusses potential advantages of increasing antioxidant and micronutrient intake Reviews hormonal influences on neurodegeneration Examines the links between protein intake and Alzheimer’s disease. Neurodegeneration and Alzheimer's Disease is an essential resource for researchers, medical practitioners, dietitians, and students with an interest in neurological diseases and their diagnosis and risk factors, as well as diet-related conditions such as diabetes and obesity. Lifestyle and diet influence neurodegeneration risk, and a better understanding of this evidence amongst health professionals will hopefully lead to greater public awareness of how to reduce the likelihood of these widespread conditions.
Author : Jean-Marc Cavaillon,Mervyn Singer
Publisher : John Wiley & Sons
Page : 1818 pages
File Size : 44,7 Mb
Release : 2018-02-20
Category : Medical
ISBN : 9783527338993
The leading reference on this topic of increasing medical relevance is unique in offering unparalleled coverage. The editors are among the most respected researchers in inflammation worldwide and here have put together a prestigious team of contributors. Starting with the molecular basis of inflammation, from cytokines via the innate immune system to the different kinds of inflammatory cells, they continue with the function of inflammation in infectious disease before devoting a large section to the relationship between inflammation and chronic diseases. The book concludes with wound and tissue healing and options for therapeutic interventions. A must have for clinicians and biomedical researchers alike.
Author : Jesus Avila,Naruhiko Sahara
Publisher : Frontiers E-books
Page : 114 pages
File Size : 40,8 Mb
Release : 2014-08-18
Category : Medicine (General)
ISBN : 9782889192618
Neurofibrillary tangles (NFTs) composed of intracellular aggregates of tau protein are a key neuropathological feature of Alzheimer’s Disease (AD) and other neurodegenerative diseases, collectively termed tauopathies. The abundance of NFTs has been reported to correlate positively with the severity of cognitive impairment in AD. However, accumulating evidences derived from studies of experimental models have identified that NFTs themselves may not be neurotoxic. Now, many of tau researchers are seeking a “toxic” form of tau protein. Moreover, it was suggested that a “toxic” tau was capable to seed aggregation of native tau protein and to propagate in a prion-like manner. However, the exact neurotoxic tau species remain unclear. Because mature tangles seem to be non-toxic component, “tau oligomers” as the candidate of “toxic” tau have been investigated for more than one decade. In this topic, we will discuss our consensus of “tau oligomers” because the term of “tau oligomers” [e.g. dimer (disulfide bond-dependent or independent), multimer (more than dimer), granular (definition by EM or AFM) and maybe small filamentous aggregates] has been used by each researchers definition. From a biochemical point of view, tau protein has several unique characteristics such as natively unfolded conformation, thermo-stability, acid-stability, and capability of post-translational modifications. Although tau protein research has been continued for a long time, we are still missing the mechanisms of NFT formation. It is unclear how the conversion is occurred from natively unfolded protein to abnormally mis-folded protein. It remains unknown how tau protein can be formed filaments [e.g. paired helical filament (PHF), straight filament and twisted filament] in cells albeit in vitro studies confirmed tau self-assembly by several inducing factors. Researchers are still debating whether tau oligomerization is primary event rather than tau phosphorylation in the tau pathogenesis. Inhibition of either tau phosphorylation or aggregation has been investigated for the prevention of tauopathies, however, it will make an irrelevant result if we don’t know an exact target of neurotoxicity. It is a time to have a consensus of definition, terminology and methodology for the identification of “tau oligomers”.
Author : Davide Moretti
Publisher : Unknown
Page : 128 pages
File Size : 49,8 Mb
Release : 2016
Category : Alzheimer's disease
ISBN : 9535126555
"The dementia challenge is the largest health effort of the times we live in. The whole society has to move to a realization of the significance of prioritization to make an attempt in the direction of mental health promotion and dementia risk reduction. New priorities for research are needed to go far beyond the usual goal of constructing a disease course-modifying medication. Moreover, a full empowerment and engagement of men and women living with dementia and their caregivers, overcoming stigma and discrimination should be promoted. The common efforts and the final aim will have to be the progress of a ''dementia-constructive'' world, where people with dementia can take advantage of equal opportunities."--Provided by publisher
Author : Rodrigo Franco,Jonathan A Doorn,Jean-Christophe Rochet
Publisher : Royal Society of Chemistry
Page : 537 pages
File Size : 40,7 Mb
Release : 2017-07-25
Category : Medical
ISBN : 9781782621881
Parkinson's Disease is the second most common neurodegenerative disorder affecting millions of people worldwide. In order to find neuroprotective strategies, a clear understanding of the mechanisms involved in the dopaminergic death of cells that progresses the disease is needed. Oxidative stress can be defined as an imbalance between the production of reactive species and the ability to detoxify them and their intermediates or by-products. Oxidative damage to lipids, proteins, and DNA has been detected in autopsies from individuals with Parkinson’s Disease and so links can be made between oxidative stress and Parkinson’s Disease pathogenesis. This book provides a thorough review of the mechanisms by which oxidative stress and redox signalling mediate Parkinson’s Disease. Opening chapters bring readers up to speed on basic knowledge regarding oxidative stress and redox signalling, Parkinson’s Disease, and neurodegeneration before the latest advances in this field are explored in detail. Topics covered in the following chapters include the role of mitochondria, dopamine metabolism, metal homeostasis, inflammation, DNA-damage and thiol-signalling. The role of genetics and gene-environment interactions are also explored before final chapters discuss the identification of potential biomarkers for diagnosis and disease progression and the future of redox/antioxidant based therapeutics. Written by recognized experts in the field, this book will be a valuable source of information for postgraduate students and academics, clinicians, toxicologists and risk assessment groups. Importantly, it presents the current research that might later lead to redox or antioxidant – based therapeutics for Parkinson’s disease.