Author: Omar Nyabi
Publisher: Leuven University Press
ISBN: 9789058674593
Category : Science
Languages : en
Pages : 122
Book Description
Alzheimer's disease is a major health problem. The disease is clinically characterized by the progressive mental decline of the patients and pathologically by the accumulation of amyloid plaques and tangles and neurodegenerative changes in the brain. The cause of the disease remains unclear but in some cases, genetic (missense) mutations in the Amyloid Precursor Protein (APP) and in the Presenilin genes (PS1 & PS2) are sufficient to initiate the whole disease cascade. All these mutations cause in essence an increase in the generation or a change of the characteristics of the AB peptide making it more prone to produce amyloid plaques. The AB peptide is generated from the APP protein and the question how Presenilin influences APP processing and AB production is the main topic of our work.
Structural and Functional Repercussions of Loss of Function and Clinical Mutants of Presenilin
Author: Omar Nyabi
Publisher: Leuven University Press
ISBN: 9789058674593
Category : Science
Languages : en
Pages : 122
Book Description
Alzheimer's disease is a major health problem. The disease is clinically characterized by the progressive mental decline of the patients and pathologically by the accumulation of amyloid plaques and tangles and neurodegenerative changes in the brain. The cause of the disease remains unclear but in some cases, genetic (missense) mutations in the Amyloid Precursor Protein (APP) and in the Presenilin genes (PS1 & PS2) are sufficient to initiate the whole disease cascade. All these mutations cause in essence an increase in the generation or a change of the characteristics of the AB peptide making it more prone to produce amyloid plaques. The AB peptide is generated from the APP protein and the question how Presenilin influences APP processing and AB production is the main topic of our work.
Publisher: Leuven University Press
ISBN: 9789058674593
Category : Science
Languages : en
Pages : 122
Book Description
Alzheimer's disease is a major health problem. The disease is clinically characterized by the progressive mental decline of the patients and pathologically by the accumulation of amyloid plaques and tangles and neurodegenerative changes in the brain. The cause of the disease remains unclear but in some cases, genetic (missense) mutations in the Amyloid Precursor Protein (APP) and in the Presenilin genes (PS1 & PS2) are sufficient to initiate the whole disease cascade. All these mutations cause in essence an increase in the generation or a change of the characteristics of the AB peptide making it more prone to produce amyloid plaques. The AB peptide is generated from the APP protein and the question how Presenilin influences APP processing and AB production is the main topic of our work.
Physiological Study of Presenilins and Baces, Two Proteases Involved in the Pathogenesis of Alzheimer's Disease
Author: Jos Tournoy
Publisher: Leuven University Press
ISBN: 9789058675262
Category : Medical
Languages : en
Pages : 124
Book Description
Publisher: Leuven University Press
ISBN: 9789058675262
Category : Medical
Languages : en
Pages : 124
Book Description
Protein Trafficking in Neurons
Author: Andrew J. Bean
Publisher: Elsevier
ISBN: 0080465897
Category : Science
Languages : en
Pages : 466
Book Description
The efficient delivery of cellular constituents to their proper location is of fundamental importance for all cells and is of particular interest to neuroscientists, because of the unique functions and complex architecture of neurons. Protein Trafficking in Neurons examines mechanisms of protein trafficking and the role of trafficking in neuronal functioning from development to plasticity to disease. The book is divided into seven sections that review mechanisms of protein transport, the role of protein trafficking in synapse formation, exo- and endocytosis, transport of receptors, trafficking of ion channels and transporters, comparison of trafficking mechanisms in neuronal vs. non-neuronal cell types, and the relationship between trafficking and neuronal diseases such as Alzheimer's, Huntington's and Prion Diseases. - Provides a comprehensive examination of membrane/protein movement in neuronal function - Sections on synapse development, synaptic transmission, and the role of trafficking in neurological disease - Includes a focus on Molecular Mechanisms - Illustrated with color summary pictures - The only book examining protein trafficking and its functional implications, written by leaders in the field
Publisher: Elsevier
ISBN: 0080465897
Category : Science
Languages : en
Pages : 466
Book Description
The efficient delivery of cellular constituents to their proper location is of fundamental importance for all cells and is of particular interest to neuroscientists, because of the unique functions and complex architecture of neurons. Protein Trafficking in Neurons examines mechanisms of protein trafficking and the role of trafficking in neuronal functioning from development to plasticity to disease. The book is divided into seven sections that review mechanisms of protein transport, the role of protein trafficking in synapse formation, exo- and endocytosis, transport of receptors, trafficking of ion channels and transporters, comparison of trafficking mechanisms in neuronal vs. non-neuronal cell types, and the relationship between trafficking and neuronal diseases such as Alzheimer's, Huntington's and Prion Diseases. - Provides a comprehensive examination of membrane/protein movement in neuronal function - Sections on synapse development, synaptic transmission, and the role of trafficking in neurological disease - Includes a focus on Molecular Mechanisms - Illustrated with color summary pictures - The only book examining protein trafficking and its functional implications, written by leaders in the field
Biochemical and Immuno-Histochemical Analysis of APP-Processing and Amyloid Pathology in Single and Multiple Transgenic Mice as Models for Alzheimer's Disease
Author: Tom V. Dooren
Publisher: Leuven University Press
ISBN: 9789058675446
Category : Medical
Languages : en
Pages : 220
Book Description
Publisher: Leuven University Press
ISBN: 9789058675446
Category : Medical
Languages : en
Pages : 220
Book Description
Generation and Characterization of a Mouse Model for a Sodium Channel Based Long QT Syndrome (LQT3)
Author: Dieter Nuyens
Publisher: Leuven University Press
ISBN: 9789058675309
Category : Medical
Languages : en
Pages : 142
Book Description
Publisher: Leuven University Press
ISBN: 9789058675309
Category : Medical
Languages : en
Pages : 142
Book Description
Expression and Function of a Serotoninergic System in the Rat Anterior Pituitary
Author: Anna-Pia Papageorgiou
Publisher: Leuven University Press
ISBN: 9789058675828
Category : Medical
Languages : en
Pages : 166
Book Description
Publisher: Leuven University Press
ISBN: 9789058675828
Category : Medical
Languages : en
Pages : 166
Book Description
A Prospective Study of Risk Factors for Low Back Disorders in Occupational Settings
Author: An van Nieuwenhuyse
Publisher: Leuven University Press
ISBN: 9789058674951
Category : Health & Fitness
Languages : en
Pages : 168
Book Description
Publisher: Leuven University Press
ISBN: 9789058674951
Category : Health & Fitness
Languages : en
Pages : 168
Book Description
Tau oligomers
Author: Jesus Avila
Publisher: Frontiers E-books
ISBN: 288919261X
Category : Medicine (General)
Languages : en
Pages : 114
Book Description
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”.
Publisher: Frontiers E-books
ISBN: 288919261X
Category : Medicine (General)
Languages : en
Pages : 114
Book Description
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”.
Biochemical Characterization and Validation of the Yeast Saccharomyces Cerevisiae as Model System for the Function of Human Protein Tau
Author: Tom Vandebroek
Publisher: Leuven University Press
ISBN: 9789058675439
Category : Science
Languages : en
Pages : 160
Book Description
Publisher: Leuven University Press
ISBN: 9789058675439
Category : Science
Languages : en
Pages : 160
Book Description
Genetic Variation and Environmental Factors in Biological and Arterial Ageing
Author: Tim Nawrot
Publisher: Leuven University Press
ISBN: 9789058674609
Category : Medical
Languages : en
Pages : 168
Book Description
Ageing, the decline in survival and bodily functions, caused by damage to macromolecules and tissues is intrinsically linked to life. Although universal and unavoidable, ageing does not occur in a uniform way. In the general population, it is actually a continuously distributed phenotype, in which genetic as well as environmental factors play an interactive role and explain the large interindividual differences between biological and chronological age. Cardiovascular disorders, which find there origins in deterioration of the structure and function of the large arteries, explain a large part of morbidity and mortality in industrialized societies. In this doctoral dissertation, the focus was on telomere length and arterial stiffness as biomarkers of biological and arterial ageing, respectively. It was investigated to what extent genetic and environmental determinants of oxidative stress and inflammation impact on the ageing process. Contents include: Introduction, Arterial ageing in cardiovascular risk prediction, Genetic and environmental factors in biological and arterial ageing, Telomere length and possible link to X chromosome, Role of smoking, oxidative stress and the -174 G/C interleukin-6 polymorphism in biological and vascular ageing, Environmental factors in arterial ageing, Blood pressure and blood selenium: a cross-sectional and a longitudinal population study, Endothelial function and outdoor temperature, General Discussion, Summary, Short Curriculum Vitae.
Publisher: Leuven University Press
ISBN: 9789058674609
Category : Medical
Languages : en
Pages : 168
Book Description
Ageing, the decline in survival and bodily functions, caused by damage to macromolecules and tissues is intrinsically linked to life. Although universal and unavoidable, ageing does not occur in a uniform way. In the general population, it is actually a continuously distributed phenotype, in which genetic as well as environmental factors play an interactive role and explain the large interindividual differences between biological and chronological age. Cardiovascular disorders, which find there origins in deterioration of the structure and function of the large arteries, explain a large part of morbidity and mortality in industrialized societies. In this doctoral dissertation, the focus was on telomere length and arterial stiffness as biomarkers of biological and arterial ageing, respectively. It was investigated to what extent genetic and environmental determinants of oxidative stress and inflammation impact on the ageing process. Contents include: Introduction, Arterial ageing in cardiovascular risk prediction, Genetic and environmental factors in biological and arterial ageing, Telomere length and possible link to X chromosome, Role of smoking, oxidative stress and the -174 G/C interleukin-6 polymorphism in biological and vascular ageing, Environmental factors in arterial ageing, Blood pressure and blood selenium: a cross-sectional and a longitudinal population study, Endothelial function and outdoor temperature, General Discussion, Summary, Short Curriculum Vitae.