Misfolding Of Amyloid Beta And Tau In Alzheimers And Other Neurodegenerative Diseases

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• Author : Jesus Avila,Naruhiko Sahara
• Publisher : Frontiers E-books
• Release Date : 2014-08-18
• Total pages : 114
• ISBN : 9782889192618
• File Size : 30,6 Mb
• Total Download : 291
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Download Tau oligomers in PDF, Epub, and Kindle

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 : Robert D. E. Sewell
• Publisher : CRC Press
• Release Date : 2007-12-03
• Total pages : 592
• ISBN : 1420007149
• File Size : 42,6 Mb
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Download Protein Misfolding in Neurodegenerative Diseases in PDF, Epub, and Kindle

Research focused on protein folding, misfolding, and aggregation is leading to major advances across biochemistry and medicine. The elucidation of a folding code is proving to be of extreme importance in the postgenomic era, where a number of orphan genes have been identified for which no clear function has yet been established. This research is starting to shed light on the molecular and biochemical basis of a number of neurodegenerative diseases of dramatic impact. Protein Misfolding in Neurodegenerative Diseases: Mechanisms and Therapeutic Strategies addresses key issues concerning protein misfolding and aggregation in neurodegenerative diseases. Building on recent developments, including the recognition of protein misfolding as both a marker and a causal agent, the text presents the work of those who are actively pursuing more effective treatments, as well as preventative measures, and a possible cure. These include the use of molecular chaperones to control misfolding and novel pharmaceuticals, as well as the potential role of various inhibitors and NSAIDS. A Comprehensive Multifaceted Examination of the Complex Causal Agents Implicated in Protein Misfolding Divided into five sections, this groundbreaking text provides up-to-date accounts for Alzheimer’s, Parkinson’s, Huntington’s, Amyotrophic Lateral Sclerosis and Transmissible Spongiform Encephalitis. It also explores the highly likelihood that multiple factors, including oxidative stress, play a role in these complex diseases.

• Author : J. Cummings,J. Hardy,M. Poncet
• Publisher : Springer Science & Business Media
• Release Date : 2006-03-30
• Total pages : 166
• ISBN : 9783540265221
• File Size : 23,5 Mb
• Total Download : 129
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Download Genotype - Proteotype - Phenotype Relationships in Neurodegenerative Diseases in PDF, Epub, and Kindle

Recent advances in understanding the role of protein dysmetabolism in neurodegeneration was the theme of the Fondation IPSEN meeting addressing Genotype-Proteotype-Phenotype relationships. Experts from international laboratories contributed to the current volume to produce a comprehensive overview of the role of protein misfolding in neurodegeneration. Links between genotype and protein characteristics and between proteotype and clinical phenomenology were discussed across diseases categories. Progress in understanding the role of abnormalities of protein metabolism may lead to the identification of biological markers relevant to disease monitoring and to the development of new therapeutic agents capable of modifying and ameliorating basic neurodegenerative mechanisms.

• Author : Uday Kishore
• Publisher : BoD – Books on Demand
• Release Date : 2013-05-15
• Total pages : 642
• ISBN : 9789535110880
• File Size : 14,6 Mb
• Total Download : 407
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Download Neurodegenerative Diseases in PDF, Epub, and Kindle

This book highlights the pathophysiological complexities of the mechanisms and factors that are likely to be involved in a range of neuroinflammatory and neurodegenerative diseases including Alzheimer's disease, other Dementia, Parkinson Diseases and Multiple Sclerosis. The spectrum of diverse factors involved in neurodegeneration, such as protein aggregation, oxidative stress, caspases and secretase, regulators, cholesterol, zinc, microglia, astrocytes, oligodendrocytes, etc, have been discussed in the context of disease progression. In addition, novel approaches to therapeutic interventions have also been presented. It is hoped that students, scientists and clinicians shall find this very informative book immensely useful and thought-provoking.

• Author : Jagan A Pillai PhD
• Publisher : Oxford University Press
• Release Date : 2016-10-17
• Total pages : 304
• ISBN : 9780190233570
• File Size : 49,9 Mb
• Total Download : 333
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Download Neurodegenerative Diseases in PDF, Epub, and Kindle

As the global population ages the impact of neurodegenerative diseases like Alzheimer's disease and Parkinson's disease are significant forces in shaping human health and quality of life in the 21st century. Insights into understanding these diseases, and knowing how to treat them are major frontiers of scientific research. Neurodegenerative Diseases: Unifying Principles is the result of a conceptual revolution over the last decade in our understanding of neurodegenerative diseases as sharing unifying features. There is an increasing appreciation of the common biological and pathological features across seemingly varied neurodegenerative diseases that entail protein misfolding dysfunction and its consequences over time. Providing an overview of this conceptual change is the main theme for the book. Conventional approach emphasize the differences among neurodegenerative disorders, here Drs. Cummings and Pillai compile the increasingly compelling evidence that these disorders share many features and that insights in one may be rapidly translated into advances in another. The goal is to accelerate understanding by showing linkages among biological, pathological, can clinical aspects of this class of diseases. This collection of 19, inter-related chapters, articulates and broadens our view of the unifying features that initiate and drive disease progression across a variety of neurodegenerative diseases over time. This book will serve as an outstanding sourcebook of insights from experts that have played key roles in this story.

• Author : Mathias Jucker,Yves Christen
• Publisher : Springer Science & Business Media
• Release Date : 2013-03-27
• Total pages : 156
• ISBN : 9783642354915
• File Size : 40,5 Mb
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Download Proteopathic Seeds and Neurodegenerative Diseases in PDF, Epub, and Kindle

The misfolding and aggregation of specific proteins is an early and obligatory event in many of the age-related neurodegenerative diseases of humans. The initial cause of this pathogenic cascade and the means whereby disease spreads through the nervous system, remain uncertain. A recent surge of research, first instigated by pathologic similarities between prion disease and Alzheimer’s disease, increasingly implicates the conversion of disease-specific proteins into an aggregate-prone b-sheet-rich state as the prime mover of the neurodegenerative process. This prion-like corruptive protein templating or seeding now characterizes such clinically and etiologically diverse neurological disorders as Alzheimer ́s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and frontotemporal lobar degeneration. Understanding the misfolding, aggregation, trafficking and pathogenicity of the affected proteins could therefore reveal universal pathomechanistic principles for some of the most devastating and intractable human brain disorders. It is time to accept that the prion concept is no longer confined to prionoses but is a promising concept for the understanding and treatment of a remarkable variety of diseases that afflict primarily our aging society. ​

• Author : Scientific American Editors
• Publisher : Scientific American
• Release Date : 2017-04-24
• Total pages : 247
• ISBN : 9781466859081
• File Size : 48,6 Mb
• Total Download : 895
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Download Fragile Brain in PDF, Epub, and Kindle

Brain disease such as Alzheimer’s and Parkinson’s affect an estimated one in six Americans and are increasing in incidence as the population ages. In this eBook, Fragile Brain: Neurodegenerative Diseases, we examine these and other conditions involving the damage and loss of neurons, including other forms of dementia, amyotrophic lateral sclerosis (ALS), chronic traumatic encephalopathy (CTE) and multiple sclerosis (MS). In “The Seeds of Dementia,” the authors discuss evidence of prions and protein misfolding as a universal culprit in Alzheimer’s and other conditions. Later, two articles by Gary Stix report on ongoing research into a cluster of Columbian families that experience early onset symptoms of Alzheimer’s. Researchers studying the genes and progression of disease in these families hope that results will reveal clues about its course and possible future remedies. In “New Movement in Parkinson’s,” the authors outline abnormal cell behavior and genetic mutations that may be behind the disease. In the study of ALS, Amy Yee examines research into why eye muscles tend to last longer than other motor neurons and what this may mean for treatment. Other pieces look at new lines of inquiry in MS, including why researchers are turning to gray matter, as opposed to white matter, as the starting point for the disease. We wrap up this collection with current preventative measures and treatments that target not only disease pathology, but also lifestyle changes as well. In “A Rare Success against Alzheimer’s,” the results of a large-scale Finnish study provide evidence that choices such as diet and exercise can help prevent cognitive decline. Although this news is far from a cure, forward movement against Alzheimer’s – and neurodegenerative disease in general – is reason for optimism. As research and evidence accumulates, we get ever closer to curative therapies that can halt the debilitation and death of neurons.

• Author : J. Robin Harris
• Publisher : Springer Science & Business Media
• Release Date : 2012-12-09
• Total pages : 654
• ISBN : 9789400754164
• File Size : 50,7 Mb
• Total Download : 608
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Download Protein Aggregation and Fibrillogenesis in Cerebral and Systemic Amyloid Disease in PDF, Epub, and Kindle

This volume of the Subcellular Biochemistry series is the result of the long-standing research interest of the editor in the molecular mechanism underlying Alzheimer’s disease and other amyloid diseases, indicated also by the earlier book in the series (Volume 38), devoted to Alzheimer’s disease. The broad coverage within the present amyloidogenesis book represents an attempt to collate current knowledge relating to the proteins and peptides involved in most of the known amyloid diseases, together with some amyloid/fibril-forming proteins and peptides that are not involved in diseases. Thus, the range of topics included is comprehensive and furthermore it was thought appropriate to include both basic science and clinical presentation of the subjects under discussion.

• Author : Yuan Jian-min,Zhou Huan-xiang
• Publisher : World Scientific
• Release Date : 2017-06-02
• Total pages : 328
• ISBN : 9789813202399
• File Size : 23,9 Mb
• Total Download : 803
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Download Biophysics And Biochemistry Of Protein Aggregation: Experimental And Theoretical Studies On Folding, Misfolding, And Self-assembly Of Amyloidogenic Peptides in PDF, Epub, and Kindle

This book reviews current research on the important processes involved in neurodegenerative diseases (e.g. Alzheimer's disease) and the peptides and proteins involved in the amyloidogenic processes. It covers the design and developments of anti-amyloid inhibitors, and gives readers a fundamental understanding of the underlying oligomerization and aggregation processes of these diseases from both computational and experimental points of view.

• Author : Alexander Sandberg
• Publisher : Linköping University Electronic Press
• Release Date : 2019-11-08
• Total pages : 51
• ISBN : 9789179299842
• File Size : 28,5 Mb
• Total Download : 878
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Download Polymorphic protein aggregation in tauopathies in PDF, Epub, and Kindle

Alzheimer’s disease(s) comprises one of the most common and costly neurodegenerative diseases. With a larger population and an increasing life expectancy, amyloid diseases (with age as one of the most prominent risk factors) will generate an even larger burden on healthcare. We know that protein misfolding is involved in the disease process but lack a complete understanding of the mechanism behind these diseases, both the sporadic and hereditary variants. It is not always known whether it is a gain-of-toxic function or loss?of?function that causes the neurodegeneration. To determine the correct diagnosis is a major challenge. If diagnosed, only a few amyloid diseases can be treated today. Amyloids are highly ordered filamentous protein aggregates with a ??sheet structure. From identical or similar amino acid sequences, a large variety of structures can be formed by different secondary and tertiary structures and by different packing of the individual filaments. This is known as fibril polymorphism. This work focuses on characterization on two proteins involved in Alzheimer’s disease and other neurodegenerative diseases, namely Amyloid?? (A?) and microtubule associated protein tau (tau). In order to investigate the properties of these proteins in vitro it is important to have protocols for production of recombinant protein that enables characterization of these aggregation prone proteins. We present protocols for recombinant expression, purification and non?denaturing fibrillation assays used in our lab to produce and analyze A?, tau and the prion protein. Development of new ligands for characterization of fibrils is an important way of investigating different fibrillary structures and characterizing and distinguishing between the different polymorphs of aggregates. We showed that the central benzene ring of the amyloid ligand X?34 can be exchanged for other heterocyclic motifs and still retain targeting of the “Congo red” binding site. The compounds do not compete with the Pittsburgh compound B (PiB) binding site on recombinant A? fibrils. We also characterized tau fibrils formed from seeding with tau aggregates from patients diagnosed with different neurodegenerative tauopathies. We use aggregation kinetics to test the seeding activity on two different sequence isoforms of tau, 0N3R and 0N4R. Fibrillation kinetics, an array of recently developed ligands (including the X?34 analogs) and electron microscopy were used to characterize different polymorphs of the tau aggregates formed by seeded templating from patient derived seeds. Our data showed that brains contain seeds with different morphologies even with in patients diagnosed with the same disease. Investigations of the rare tau mutant G273R found in a patient with a presumed tauopathy also highlights the problem with proper diagnostics. Our results reveal that in vitro this mutation change the binding properties of 0N4R tau to the cytoskeletal proteins microtubule and F?actin. Furthermore, we could show that when seeded, the fibril formation seeding activity followed a sequence similarity dependent manner. In fibrils formed during heparin-induced aggregation we can be distinguished between wild type and mutant tau as they form fibrils with different thickness. Our in vitro biophysical data support that the G237R mutant is causing a 4R tauopathy. The work in this thesis increase our knowledge in the field of tau aggregation and tau fibril polymorphism. En av de vanligaste och mest kostsamma sjukdomarna är den nervdödande Alzheimers sjukdom. Med en större population och ökad förväntad livslängd kommer amyloida sjukdomar, som har ålder som den viktigaste riskfaktorn, att generera en ökad börda för sjukvården. Vi saknar en fullständig förståelse för mekanismerna bakom dessa sjukdomar både för de sporadiska och ärftliga varianterna. Man vet att felveckade proteiner är inblandade i dessa sjukdomar. Det är inte alltid känt hur den felveckade formen av ett protein alstrar en toxisk funktion eller om det är en förlust av dennas funktion som orsakar nervdöden. Att kunna fastställa en korrekt diagnos är en stor utmaning för forskarvärlden idag. Även när en korrekt diagnos kan ställas är det endast ett fåtal amyloida sjukdomar som kan behandlas idag. Amyloider är mycket välordnade filamentösa proteinaggregat med ?-flakstruktur. Från identiska eller liknande aminosyrasekvenser kan ett stort antal strukturer bildas med olika sekundär- och tertiär struktur och olika packning av individuella filament. Vi kallar detta för strukturell polymorfism. Det här arbetet fokuserar på karakterisering av två proteiner involverade i Alzheimers sjukdom och andra neurodegenerativa sjukdomar nämligen Amyloid ? (A?) och mikrotubuli associerade protein tau (tau). För att kunna undersöka egenskaperna hos dessa proteiner är det viktigt att ha protokoll för produktion av rekombinant protein för att kunna karakterisera dessa aggregeringsbenägna proteiner. Vi utvecklade protokoll för rekombinant utryck, rening och icke-denaturerande fibrilleringsanalyser som används i vårt labb för att producera och analysera A?, tau och prionproteinet. Utveckling av nya ligander för karakterisering av fibriller är en viktig väg för att undersöka olika fibrillstrukturer och för karakterisering och för att kunna särskilja mellan olika polymorfer av aggregat. I det här arbetet visas att den centrala bensenringen hos amyloidliganden X-34 kan bytas ut mot andra heterocykliska motiv och fortfarande behålla sin specificitet mot ”Congo röd” bindnings-sätet utan att konkurrera med Pittsburgh compound B (PiB) bindnings-säte på rekombinanta A? fibriller. Vi karaktäriserade också tau fibriller bildade via ympning, så kallad seeding, med tau aggregat isolerade från patienter diagnosticerade med olika nervdödande taupatier. Vi använder aggregerings kinetik för att testa seedningsförmåga på två olika sekvens isoformer av tau. Nyligen utvecklade ligander (inkluderat X-34 analoger) och elektronmikroskopi användes för att karakterisera de olika polymorferna av tau aggregaten. Våra data påvisar att olika patienter bär på olika seeds, det vill säga olika polymorpher. Även mellan patienter med samma diagnos finns skillnader. Undersökningar av den ovanliga tau mutationen G273R understryker också problemet med fastställandet av korrekt diagnos. Våra resultat från provrörsexperiment avslöjar att den här mutationen ändrar bindningsegenskaperna av 0N4R tau till cytoskelettproteinerna mikrotubulin och F-aktin. Vi kunde ytterligare visa att när fibrilleringsreaktionen seedades så följde det en sekvenslikhetsberoende mekanism. Fibrerna som bildas under heparininducering kan skiljas åt mellan normalt och muterat tau genom att de har olika tjocklek. Våra biofysikaliska data stödjer att G273R tau mutationen kan orsaka en 4R tauopati. Arbetet i denna avhandling ökar vår kunskap inom området tau-aggregering och tau fibrilpolymorfism.

• Author : Yohei Shibuya
• Publisher : Unknown
• Release Date : 2015
• Total pages : 348
• ISBN : OCLC:915962559
• File Size : 36,6 Mb
• Total Download : 777
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Download ACAT1 Blockage Stimulates Autophagy to Ameliorate Alzheimer's Disease in PDF, Epub, and Kindle

Alzheimer's disease (AD) is a progressive neurodegenerative disease and the most common cause of dementia in the aging population. Currently, there is no cure for AD. The hallmark of AD consists of extracellular amyloid plaques, mainly composed of amyloid beta (A[beta]) peptides (especially A[beta]1-42), and neurofibrillary tangles, mainly composed of hyperphosphorylated tau. A[beta] and tau can interact with each other synergistically to trigger neurotoxicity. Autophagy is a lysosomal degradation process that mediates the cellular clearance of misfolded/aggregated proteins/peptides including A[beta] and tau. Malfunctions in autophagy have been observed in several neurodegenerative diseases, and it has been proposed that promoting cellular autophagy may be an effective strategy to treat AD and other related neurodegenerative diseases. Acyl-CoA: cholesterol acyltransferase (ACAT) converts free cholesterol to cholesteryl esters and plays important roles in cellular cholesterol homeostasis. Previous work from this and other laboratories showed that blocking ACAT1 decreases amyloidopathy in cell culture and in mouse models for AD. These studies suggest the potential therapeutic use of ACAT1 blockage to treat AD. However, the mechanism(s) responsible for the beneficial actions of blocking ACAT1 to treat AD remained not well understood. Microglia play essential roles in the proteolytic clearance of A[beta] peptides. In Chapter 2, I show that Acat1 gene KO in mouse increases phagocytic uptake of oligomeric A[beta]1-42 and stimulates lysosomal A[beta]1-42 degradation in cultured microglia and in vivo. Additional results show that Acat1 gene KO or a specific ACAT1 inhibitor K604 stimulates autophagosome formation and transcription factor EB-mediated lysosomal proteolysis. In Chapter 3, I show that in murine neuroblastoma cells ectopically expressing human tau, and in primary neurons isolated from triple transgenic AD mice, ACAT1 blockage increases autophagosome formation, increases lysosomal enzyme gene expression, and decreases human tau protein content, without affecting endogenous mouse tau protein content. A common event that occurs in several prevalent neurodegenerative diseases, is the prominent presence of specific misfolded/aggregated proteins/peptides in certain regions of the CNS. The cellular clearance of misfolded/aggregated proteins/peptides involves autophagy-mediated lysosomal proteolysis. My results suggest that blocking ACAT1 may provide a novel way to benefit several neurodegenerative diseases in general.

• Author : Michael S. Wolfe
• Publisher : Academic Press
• Release Date : 2018-03-29
• Total pages : 560
• ISBN : 9780128113059
• File Size : 24,9 Mb
• Total Download : 680
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Download The Molecular and Cellular Basis of Neurodegenerative Diseases in PDF, Epub, and Kindle

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 : Sonia Do Carmo,A. Claudio Cuello,Maria Grazia Spillantini
• Publisher : Frontiers Media SA
• Release Date : 2021-11-12
• Total pages : 268
• ISBN : 9782889716258
• File Size : 53,9 Mb
• Total Download : 592
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Download Tau Pathology in Neurological Disorders in PDF, Epub, and Kindle

PDF book entitled Tau Pathology in Neurological Disorders written by Sonia Do Carmo,A. Claudio Cuello,Maria Grazia Spillantini and published by Frontiers Media SA which was released on 2021-11-12 with total hardcover pages 268, the book become popular and critical acclaim.

• Author : Forum on Neuroscience and Nervous System Disorders,Board on Health Sciences Policy,Institute of Medicine
• Publisher : National Academies Press
• Release Date : 2013-12-26
• Total pages : 0
• ISBN : 0309285674
• File Size : 31,6 Mb
• Total Download : 596
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Download Neurodegeneration in PDF, Epub, and Kindle

Neurodegeneration: Exploring Commonalities Across Diseases is the summary of a workshop hosted by the Institute of Medicine\'s (IOM\'s) Forum on Neuroscience and Nervous System Disorders in Spring 2012 to explore commonalities across neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD). Participants from academia; pharmaceutical and biotechnology industries; government agencies such as the National Institutes of Health and the U.S. Department of Veterans Affairs (VA); patient advocacy groups; and private foundations presented and identified potential opportunities for collaboration across the respective research and development communities. This report identifies and discusses commonalities related to genetic and cellular mechanisms, identifies areas of fundamental science needed to facilitate therapeutics development, and explores areas of potential collaboration among the respective research communities. Neurodegenerative diseases, such as Alzheimer\'s disease, Parkinson\'s disease, ALS, and FTD, are becoming increasingly prevalent in the United States due to an aging population. Implications are grave for quality of life and health care costs. Research on neurodegenerative diseases has expanded greatly over the past four decades. Nevertheless, fundamental questions remain about the biology of these diseases, and further insights into the mechanisms of these diseases would help to inform the development of effective means to prevent and to efficiently treat them. Recent findings have revealed certain commonalities in genetic and cellular mechanisms across neurodegenerative diseases. These findings suggest that it might be valuable - at least in some cases - to change the traditional way of studying these diseases by no longer seeing each as an independent entity, but rather as clinical variants of common cellular and molecular biological defects. This approach could help enhance basic scientific understanding of neurodegenerative disease, and could help with the development of biomarkers and new therapeutics.

• Author : Anonim
• Publisher : Academic Press
• Release Date : 2012-05-22
• Total pages : 498
• ISBN : 9780123858849
• File Size : 40,5 Mb
• Total Download : 206
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Download Molecular Biology of Neurodegenerative Diseases in PDF, Epub, and Kindle

Neurodegenerative diseases result in progressive degeneration and / or death of nerve cells which leads to problems with movement and mental functioning. Examples include Parkinson’s, Alzheimer’s and Huntington’s disease. Much research is taking place to try to identify ways to prevent or lessen the impact of these diseases. This volume reviews the latest research and developments in the molecular biology of neurodegenerative diseases. Contributions from leading authorities Informs and updates on all the latest developments in the field

• Author : Anonim
• Publisher : ScholarlyEditions
• Release Date : 2012-12-10
• Total pages : 63
• ISBN : 9781464974274
• File Size : 33,6 Mb
• Total Download : 646
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Download Neurodegenerative Diseases: New Insights for the Healthcare Professional: 2012 Edition in PDF, Epub, and Kindle

Neurodegenerative Diseases: New Insights for the Healthcare Professional / 2012 Edition is a ScholarlyBrief™ that delivers timely, authoritative, comprehensive, and specialized information about Neurodegenerative Diseases in a concise format. The editors have built Neurodegenerative Diseases: New Insights for the Healthcare Professional / 2012 Edition on the vast information databases of ScholarlyNews.™ You can expect the information about Neurodegenerative Diseases in this eBook to be deeper than what you can access anywhere else, as well as consistently reliable, authoritative, informed, and relevant. The content of Neurodegenerative Diseases: New Insights for the Healthcare Professional / 2012 Edition has been produced by the world’s leading scientists, engineers, analysts, research institutions, and companies. All of the content is from peer-reviewed sources, and all of it is written, assembled, and edited by the editors at ScholarlyEditions™ and available exclusively from us. You now have a source you can cite with authority, confidence, and credibility. More information is available at http://www.ScholarlyEditions.com/.

• Author : Patrick A. Lewis,Jennifer E. Spillane
• Publisher : Academic Press
• Release Date : 2018-11-16
• Total pages : 274
• ISBN : 9780128110706
• File Size : 33,6 Mb
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Download The Molecular and Clinical Pathology of Neurodegenerative Disease in PDF, Epub, and Kindle

The Molecular and Clinical Pathology of Neurodegenerative Disease brings together in one volume our current understanding of the molecular basis of neurodegeneration in humans, targeted at neuroscientists and graduate students in neuroscience, and the biomedical and biological sciences. Bringing together up-to-date molecular biology data with clinical evidence, this book sheds a light on common molecular mechanisms that underlie many different neurodegenerative diseases and addresses the molecular pathologies in each. The combined research and clinical background of the authors provides a unique perspective in relating clinical experiences with the molecular understanding needed to examine these diseases and is a must-read for anyone who wants to learn more about neurodegeneration. Provides an up-to-date summary of neurodegeneration at a molecular, cellular, and tissue level for the most common human disorders Describes the clinical background and underlying molecular processes for Alzheimer’s disease, Parkinson’s, Prion, Motor Neuron, Huntington’s, and Multiple Sclerosis Highlights the state-of-the-art treatment options for each disorder Details examples of relevant cutting edge experimental systems, including genome editing and human pluripotent stem cell-derived neuronal models

• Author : Debomoy K. Lahiri
• Publisher : Bentham Science Publishers
• Release Date : 2014-09-29
• Total pages : 463
• ISBN : 9781608058525
• File Size : 53,6 Mb
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Download Advances in Alzheimer's Research in PDF, Epub, and Kindle

Alzheimer’s disease (AD) is currently recognized as an untreatable, progressive, degenerative and terminal disease that is global – afflicting over 36 million people worldwide, with the number growing in an unabated and frightening manner. The goal of the series Advances in Alzheimer’s Research , with Volumes 1 and 2, is to provide an integrated approach to AD from basic and clinical research and to highlight the valuable information in order to unravel the origin, pathogenesis and prevention of AD. The aim of this book is to both capture and discuss improvements toward the diagnosis and potential treatment of AD by both established and novel strategies. This book series, including the Volume 2, provides an important mechanism to bring under the same roof a variety of scientific interests and expertise to specifically focus on AD and related dementias. The fullest attempt has been made to disseminate the most current knowledge on recent advances in potential therapy of AD.

• Author : Illana Gozes
• Publisher : Academic Press
• Release Date : 2016-12-30
• Total pages : 342
• ISBN : 9780128037126
• File Size : 24,9 Mb
• Total Download : 691
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Download Neuroprotection in Alzheimer's Disease in PDF, Epub, and Kindle

Neuroprotection in Alzheimer’s Disease offers a translational point-of-view from both basic and clinical standpoints, putting it on the cusp for further clinical development with its emphasis on nerve cell protection, including the accumulation of knowledge from failed clinical trials and new advances in disease management. This book brings together the latest findings, both basic, and clinical, under the same cover, making it easy for the reader to obtain a complete overview of the state-of-the-field and beyond. Alzheimer's disease is the most common form of dementia, accounting for 60 to 80 percent of dementia cases. It is a progressive brain disease that slowly destroys memory, thinking skills, and eventually, even the ability to carry out the simplest tasks. It is characterized by death of synapses coupled to death nerve cells and brain degeneration which is manifested by loss of cognitive abilities. Understanding neuroprotection in Alzheimer’s disease will pave the path to better disease management and novel therapeutics. Comprehensive reference detailing neuroprotection in Alzheimer’s Disease, with details on nerve cell protection and new advances in disease management Combines the knowledge and points-of-view of both medical doctors and basic scientists, putting the subject at the forefront for further clinical development Edited by one of the leading researchers in Alzheimer’s Disease

• Author : Hardy J. Rideout
• Publisher : Springer
• Release Date : 2017-03-28
• Total pages : 271
• ISBN : 9783319499697
• File Size : 43,7 Mb
• Total Download : 114
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Download Leucine-Rich Repeat Kinase 2 (LRRK2) in PDF, Epub, and Kindle

This is the first book to assemble the leading researchers in the field of LRRK2 biology and neurology and provide a snapshot of the current state of knowledge, encompassing all major aspects of its function and dysfunction. The contributors are experts in cell biology and physiology, neurobiology, and medicinal chemistry, bringing a multidisciplinary perspective on the gene and its role in disease. The book covers the identification of LRRK2 as a major contributor to the pathogenesis of Parkinson's Disease. It also discusses the current state of the field after a decade of research, putative normal physiological roles of LRRK2, and the various pathways that have been identified in the search for the mechanism(s) of its induction of neurodegeneration.

• Author : Dennis J. Selkoe,David Michael Holtzman,Eckhard Mandelkow
• Publisher : Cold Spring Harbor Perspective
• Release Date : 2012
• Total pages : 0
• ISBN : 1936113449
• File Size : 52,5 Mb
• Total Download : 545
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Download The Biology of Alzheimer Disease in PDF, Epub, and Kindle

Alzheimer disease causes the gradual deterioration of cognitive function, including severe memory loss and impairments in abstraction and reasoning. Understanding the complex changes that occur in the brain as the disease progressesincluding the accumulation of amyloid plaques and neurofibrillary tanglesis critical for the development of successful therapeutic approaches. Written and edited by leading experts in the field, this collection from Cold Spring Harbor Perspectives in Medicine includes contributions covering all aspects of Alzheimer disease, from our current molecular understanding to therapeutic agents that could be used to treat and, ultimately, prevent it. Contributors discuss the biochemistry and cell biology of amyloid -protein precursor (APP), tau, presenilin, -secretase, and apolipoprotein E and their involvement in Alzheimer disease. They also review the clinical, neuropathological, imaging, and biomarker phenotypes of the disease; genetic alterations associated with the disorder; and epidemiological insights into its causation and pathogenesis. This comprehensive volume, which includes discussions of therapeutic strategies that are currently used or under development, is a vital reference for neurobiologists, cell biologists, pathologists, and other scientists pursuing the biological basis of Alzheimer disease, as well as investigators, clinicians, and students interested in its pathogenesis, treatment, and prevention.