Modelling The Tau Pathology Of Alzheimer S Disease In Vivo And In Vitro
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Modelling The Tau Pathology Of Alzheimer S Disease In Vivo And In Vitro
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Author : Alessandra Ferrari
language : en
Publisher:
Release Date : 2002
Modelling The Tau Pathology Of Alzheimer S Disease In Vivo And In Vitro written by Alessandra Ferrari and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2002 with categories.
Tau Protein
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Author : Caroline Smet-Nocca
language : en
Publisher: Springer Nature
Release Date :
Tau Protein written by Caroline Smet-Nocca and has been published by Springer Nature this book supported file pdf, txt, epub, kindle and other format this book has been release on with categories.
Tau Biology
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Author : Akihiko Takashima
language : en
Publisher: Springer Nature
Release Date : 2020-02-24
Tau Biology written by Akihiko Takashima and has been published by Springer Nature this book supported file pdf, txt, epub, kindle and other format this book has been release on 2020-02-24 with Medical categories.
This book presents essential studies and cutting-edge research results on tau, which is attracting increasing interest as a target for the treatment of Alzheimer's disease. Tau is well known as a microtubule-associated protein that is predominantly localized in the axons of neurons. In various forms of brain disease, neuronal loss occurs, with deposition of hyperphosphorylated tau in the remaining neurons. Important questions remain regarding the way in which tau forms hyperphosphorylated and fibrillar deposits in neurons, and whether tau aggregation represents the toxic pathway leading to neuronal death. With the help of new technologies, researchers are now solving these long-standing questions. In this book, readers will find the latest expert knowledge on all aspects of tau biology, including the structure and role of the tau molecule, tau localization and function, the pathology, drivers, and markers of tauopathies, tau aggregation, and treatments targeting tau. Tau Biology will be an invaluable source of information and fresh ideas for those involved in the development of more effective therapies and for all who seek a better understanding of the biology of the aging brain.
Computational And Experimental Studies In Alzheimer S Disease
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Author : Kunal Bhattacharya
language : en
Publisher: CRC Press
Release Date : 2024-03-29
Computational And Experimental Studies In Alzheimer S Disease written by Kunal Bhattacharya and has been published by CRC Press this book supported file pdf, txt, epub, kindle and other format this book has been release on 2024-03-29 with Science categories.
This reference book compiles the recent advances in computational and experimental modelling to screen and manage Alzheimer’s disease. It covers basic etiopathology and various in vitro and in vivo strategies of disease intervention. The book discusses how computer-aided drug design approaches reduce costs and increase biological test efficiency. It reviews the screening for anti-Alzheimer drugs and biomarker analysis of disease inhibitors. The book also explores mechanistic aspects of neurodegeneration and the use of natural products as therapeutics for Alzheimer’s disease. Key features: Elaborates on the computational modelling of protein target inhibitors as anti-Alzheimer’s agents Explains the role of phytomolecules and natural products in Alzheimer’s therapy Reviews preclinical ways to assess drugs focusing on Alzheimer’s disease Covers biomarker analysis for Alzheimer’s disease Discusses the onset and progression of Alzheimer’s disease The book is meant for professionals, researchers, and students of neuroscience, psychology, and computational neurosciences.
The Role Of Glial Glutamate Transporter And Its Impact On Amyloid Beta And Tau Pathology In Alzheimer S Disease
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Author :
language : en
Publisher:
Release Date : 2017
The Role Of Glial Glutamate Transporter And Its Impact On Amyloid Beta And Tau Pathology In Alzheimer S Disease written by and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2017 with categories.
Alzheimer's disease (AD) is the leading cause of dementia among elderly in the United States. There is no effective treatment available, in part due to lack of understanding of the full spectrum of the disease mechanisms. Brain is structured in highly heterogeneous and complex way, and the number of different cell lineages, such as neurons, astrocytes, microglia, oligodendrocytes, perivascular macrophages, and capillary endothelial cells, interact with each other and functionally integrate into one highly hierarchical and organized unit. Traditionally, neurodegeneration has been centered for investigation on neurodegenerative diseases like AD. However, recent rapidly growing evidence strongly implicates the pathogenic involvement of non-neuronal cell lineages, such as astrocytes and microglia, and this work may uncover key disease mechanisms. The purpose of this dissertation is to elucidate the role of glutamate transporter 1 (GLT-1) primarily expressed in astrocytes in the progression or initiation of AD pathology. In humans, its loss is evident even in early or prodromal stages of AD and correlates well with cognitive impairment. The loss of GLT-1 causes glutamate dyshomeostasis in the synaptic cleft, which eventually leads to glutamate-induced excitotoxicity and neurodegeneration. While glutamate excitotoxicity has long been a suspected cause of progressive neurodegeneration in AD, it remains unclear whether the loss of the glutamate transporter directly contributes to the pathological buildup of amyloid ß (Aß) and neurofibrillary tau tangles (NFTs) - two key pathological hallmarks of AD. Thus, we hypothesize that the Aß-induced GLT-1 downregulation links Aß pathology to tau pathology, synaptic loss, and cognitive decline. To test this hypothesis, we utilized both in vitro and in vivo models of AD and thoroughly performed biochemical and histopathological examinations. We show an age-dependent decrease of GLT-1 in animal models and GLT-1 decrease in human hippocampal samples. In addition, pharmacological restoration of GLT-1 can ameliorate AD-like pathology in an animal model of AD. We also present a possible molecular mechanism that regulates GLT-1 independent of Aß. The contribution of this research includes a better understanding on the role of astrocyte dysfunction in the early stages of AD and its consequences on the progression of the disease.
Alzheimer S Disease Theranostics
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Author : Magisetty Obulesu
language : en
Publisher: Academic Press
Release Date : 2019-01-20
Alzheimer S Disease Theranostics written by Magisetty Obulesu and has been published by Academic Press this book supported file pdf, txt, epub, kindle and other format this book has been release on 2019-01-20 with Medical categories.
Alzheimer’s Disease Theranostics discusses the latest information on recent theranostic avenues for both the diagnosis and treatment of Alzheimer’s patients. It presents the pros and cons of the probable mechanistic role of nanoparticles in crossing the blood-brain barrier and improving disease symptoms. Finally, it highlights the merits of existing maneuvers and suggests perspectives to aid in future developments. Despite the difficulty of drug delivery to the brain, there are some nanoparticulate platforms demonstrating promise in treating neurodegenerative disorders such as Alzheimer’s disease. Manifold theranostic maneuvers include antioxidants, natural bioactive compounds, gene therapy, and nanotechnological approaches, all of which are discussed in this important work. Examines various theranostic applications for the diagnosis and treatment of Alzheimer’s disease Features a comprehensive overview of nanoparticle therapeutics in the area and use of antioxidants Assesses the common challenges and lessons learned from blood-brain barrier challenges, viral vector approaches and mitochondria-targeted therapeutics
Neurodegeneration
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Author : Dennis Dickson
language : en
Publisher: John Wiley & Sons
Release Date : 2011-09-09
Neurodegeneration written by Dennis Dickson and has been published by John Wiley & Sons this book supported file pdf, txt, epub, kindle and other format this book has been release on 2011-09-09 with Medical categories.
Most textbooks on neurodegenerative disorders have used a classification scheme based upon either clinical syndromes or anatomical distribution of the pathology. In contrast, this book looks to the future and uses a classification based upon molecular mechanisms, rather than clinical or anatomical boundaries. Major advances in molecular genetics and the application of biochemical and immunocytochemical techniques to neurodegenerative disorders have generated this new approach. Throughout most of the current volume, diseases are clustered according to the proteins that accumulate within cells (e.g. tau, α-synuclein and TDP-43) and in the extracellular compartments (e.g. β-amyloid and prion proteins) or according to a shared pathogenetic mechanism, such as trinucleotide repeats, that are a feature of specific genetic disorders. Chapters throughout the book conform to a standard lay-out for ease of access by the reader and are written by a panel of International Experts Since the first edition of this book, major advances have been made in the discovery of common molecular mechanisms between many neurodegenerative diseases most notably in the frontotemporal lobar degenerations (FTLD) and motor neuron disease or amyotrophic lateral sclerosis. This book will be essential reading for clinicians, neuropathologists and basic neuroscientists who require the firm up-to-date knowledge of mechanisms, diagnostic pathology and genetics of Neurodegenerative diseases that is required for progress in therapy and management.
Protopine And Its Derivatives Mitigate Tau Pathology Via Histone Deacetylase 6 Inhibition In Alzheimer S Disease Models
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Author : Sravan G. S. Sreenivasa Murthy
language : en
Publisher:
Release Date : 2021
Protopine And Its Derivatives Mitigate Tau Pathology Via Histone Deacetylase 6 Inhibition In Alzheimer S Disease Models written by Sravan G. S. Sreenivasa Murthy and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2021 with Alzheimer's disease categories.
The low success rates of clinical trials for Alzheimer's Disease (AD) medicament has demanded for safer and effective novel drugs. In AD, neurofibrillary tangles (NFTs) enriched with hyperphosphorylated tau is the causative factor for memory and cognitive imbalance. Emerging evidence has demonstrated an impairment of the ubiquitin-proteasomal system (UPS) upon accumulation of hyperphosphorylated tau. Histone deacetylase 6 (HDAC6) is a vital enzyme involved in tau hyperphosphorylation and cognitive dysfunction in AD animal models. Furthermore, previous studies have shown that downregulating HDAC6 activity and enhancing carboxy-terminus of HSC70 interacting protein (CHIP) mitigates tau pathology in AD. In the current study, we have elucidated the cognition-enhancing effects and the underlying mechanisms of isoquinoline alkaloid, Protopine (PRO), isolated from traditional Chinese medicine, Corydalis yanhusuo. PRO specifically reduced the hyperphosphorylated tau and alleviated the learning and memory dysfunction in triple transgenic 3xTg-AD mice and mutant tau overexpressed P301S tau mice models. Molecular docking, solid-phase binding, and fluorometric assays suggested that PRO directly binds to the catalytic domain 1 (CD1) of HDAC6 and inhibits its activity. PRO enhanced the expression of molecular chaperones and CHIP E3 ubiquitin ligase in vitro and in vivo, which further promoted the degradation of ubiquitinated tau via the ubiquitin-proteasomal system (UPS). To develop more potent HDAC6 inhibitors with optimized brain bioavailability for treating AD, a chemical derivative of PRO, termed PRO-Br, was synthesized. The physicochemical charecteristics were evaluated by Nuclear magnetic resonance spectroscopy and tandem mass spectrometry. In 3xTg-AD and P301S mice models, PRO-Br specifically promoted the i degradation of sarkosyl insoluble tau. Additionally, immunohistochemical results demonstrated that PRO-Br significantly reduced the hyperphosphosphorylated tau in both AD model mice. The fluorometric assay showed that PRO-Br decreased HDAC6 activity in a dose-dependent manner. Altogether, our findings demonstrated that 1) PRO-Br is a better blood-brain barrier permeable compound than PRO; 2) PRO-Br is a better inhibitor of HDAC6 activity, compared to PRO; 3) PRO and PRO-Br can enhance the expression of molecular chaperones and specifically promote the degradation of pathological hyperphosphorylated tau in 3xTg-AD as well as P301S tau AD models; 4) PRO and PRO-Br can mitigate the memory and cognitive impairment in both AD model mice; and 5) PRO and PRO-Br can be developed into potential drugs for treating AD.
Alzheimer S Disease
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Author : George Perry
language : en
Publisher: IOS Press
Release Date : 2006
Alzheimer S Disease written by George Perry and has been published by IOS Press this book supported file pdf, txt, epub, kindle and other format this book has been release on 2006 with Medical categories.
"This is the book edition of the Journal of Alzheimer's Disease, Volume 9, No.3 Supplement (2006)"--T.p. verso.
Tau Oligomers
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Author : Jesus Avila
language : en
Publisher: Frontiers E-books
Release Date : 2014-08-18
Tau Oligomers written by Jesus Avila and has been published by Frontiers E-books this book supported file pdf, txt, epub, kindle and other format this book has been release on 2014-08-18 with Medicine (General) categories.
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”.