neurodegenerative disorders loss function (21 risultati)

Hardcover. Condizione: Very Good. No Jacket. Former library book; May have limited writing in cover pages. Pages are unmarked. ~ ThriftBooks: Read More, Spend Less.

Condizione: Very Good. 2001st Edition. Used book that is in excellent condition. May show signs of wear or have minor defects.

Hardcover. Condizione: Très bon. Ancien livre de bibliothèque. Edition 2001. Ammareal reverse jusqu'à 15% du prix net de cet article à des organisations caritatives. ENGLISH DESCRIPTION Book Condition: Used, Very good. Former library book. Edition 2001. Ammareal gives back up to 15% of this item's net price to charity organizations.

Condizione: Good. Your purchase helps support Sri Lankan Children's Charity 'The Rainbow Centre'. Ex-library, so some stamps and wear, and may have sticker on cover, but in good overall condition. Our donations to The Rainbow Centre have helped provide an education and a safe haven to hundreds of children who live in appalling conditions.

Condizione: New. In.

Condizione: New. pp. xiv + 190.

Taschenbuch. Condizione: Neu. Neurodegenerative Disorders: Loss of Function Through Gain of Function | K. Beyreuther (u. a.) | Taschenbuch | xiv | Englisch | 2010 | Springer Spektrum | EAN 9783642074486 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Buch. Condizione: Neu. Neuware -Fondation Ipsen sponsored a meeting in Paris in February 2000 on the emerging paradigm-shift in our understanding of the major degenerative diseases which affect the aging human brain. This book sumarizes our deliberations on some of these major neurodegenerative diseases that are characterized by protein depos its, and that are due to the pathogenic gain of function of an otherwise normal neuronal protein. For each of the major human neurodegenerative diseases covered in this book -the most prominent being Alzheimer's disease -experimental models are described, including cell culture systems and animal models which range from the round worm, Caenorhabditis elegans, the fruitfly, Drosophila melanogaster, to rodents. Remarkably, in the sporadic forms of these human diseases, only a minor change in the level of production or turn-over of the relevant proteins is sufficient to cause disease in late adult-hood. Neurodegeneration in Alzheimer's disease, for example, usually results in symptoms and signs in the seventh to eighth decades. In contrast, the development of protein deposits in transgenic mice over-expressing the corresponding disease gene parallels the genetic forms of the human diseases in regard to its manifestation occuring half-way through its normal life-span, i. e. about 50 years in humans (the so-called 'presenium') and 9 to 12 months in the mouse. Nevertheless, these models have served to elu cidate many of the pathways underlying the human disease processes, for instance clarifying the neuronal origin of parenchymal and perivascular amyloid in Alzheimer's disease and Creutzfeldt-Jakob disease. 212 pp. Englisch.

Taschenbuch. Condizione: Neu. Druck auf Anfrage Neuware - Printed after ordering - A fundamental change is occurring in the understanding of the major neurodegenerative disorders. Protein aggregation is a common emerging theme in diseases as diverse as Alzheimer's, Creutzfeld-Jakob, Parkinson's, and amyotrophic lateral sclerosis. If valid, then a small number of diagnostic and rational therapeutic strategies will emerge over the next few years, based on the common theme of modulation of the production, turnover and deposition of these aggregating proteins. The book provides insights into the cellular and animal models of these diseases, and how the molecular basis of neurodegeneration has become the preferred target of therapy.

Buch. Condizione: Neu. Druck auf Anfrage Neuware - Printed after ordering - Fondation Ipsen sponsored a meeting in Paris in February 2000 on the emerging paradigm-shift in our understanding of the major degenerative diseases which affect the aging human brain. This book sumarizes our deliberations on some of these major neurodegenerative diseases that are characterized by protein depos its, and that are due to the pathogenic gain of function of an otherwise normal neuronal protein. For each of the major human neurodegenerative diseases covered in this book -the most prominent being Alzheimer's disease -experimental models are described, including cell culture systems and animal models which range from the round worm, Caenorhabditis elegans, the fruitfly, Drosophila melanogaster, to rodents. Remarkably, in the sporadic forms of these human diseases, only a minor change in the level of production or turn-over of the relevant proteins is sufficient to cause disease in late adult-hood. Neurodegeneration in Alzheimer's disease, for example, usually results in symptoms and signs in the seventh to eighth decades. In contrast, the development of protein deposits in transgenic mice over-expressing the corresponding disease gene parallels the genetic forms of the human diseases in regard to its manifestation occuring half-way through its normal life-span, i. e. about 50 years in humans (the so-called 'presenium') and 9 to 12 months in the mouse. Nevertheless, these models have served to elu cidate many of the pathways underlying the human disease processes, for instance clarifying the neuronal origin of parenchymal and perivascular amyloid in Alzheimer's disease and Creutzfeldt-Jakob disease.

Hardcover. Condizione: Brand New. 1st edition. 189 pages. 9.50x6.50x0.25 inches. In Stock.

Paperback. Condizione: Brand New. reprint edition. 204 pages. 9.25x6.10x0.49 inches. In Stock.

Paperback. Condizione: Like New. Like New. Ships from Multiple Locations. book.

Hardcover. Condizione: Like New. Like New. book.

Taschenbuch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -A fundamental change is occurring in the understanding of the major neurodegenerative disorders. Protein aggregation is a common emerging theme in diseases as diverse as Alzheimer's, Creutzfeld-Jakob, Parkinson's, and amyotrophic lateral sclerosis. If valid, then a small number of diagnostic and rational therapeutic strategies will emerge over the next few years, based on the common theme of modulation of the production, turnover and deposition of these aggregating proteins. The book provides insights into the cellular and animal models of these diseases, and how the molecular basis of neurodegeneration has become the preferred target of therapy. 208 pp. Englisch.

Condizione: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. The natural history of Alzheimer s Disease: minding the gaps in understanding the mechanisms of neurodegeneration.-Pathological mechanisms in Huntingdon s Disease and other polyglutamine expansion diseases.-Prion protein biogenesis: implications for neurode.

Buch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -Fondation Ipsen sponsored a meeting in Paris in February 2000 on the emerging paradigm-shift in our understanding of the major degenerative diseases which affect the aging human brain. This book sumarizes our deliberations on some of these major neurodegenerative diseases that are characterized by protein depos its, and that are due to the pathogenic gain of function of an otherwise normal neuronal protein. For each of the major human neurodegenerative diseases covered in this book -the most prominent being Alzheimer's disease -experimental models are described, including cell culture systems and animal models which range from the round worm, Caenorhabditis elegans, the fruitfly, Drosophila melanogaster, to rodents. Remarkably, in the sporadic forms of these human diseases, only a minor change in the level of production or turn-over of the relevant proteins is sufficient to cause disease in late adult-hood. Neurodegeneration in Alzheimer's disease, for example, usually results in symptoms and signs in the seventh to eighth decades. In contrast, the development of protein deposits in transgenic mice over-expressing the corresponding disease gene parallels the genetic forms of the human diseases in regard to its manifestation occuring half-way through its normal life-span, i. e. about 50 years in humans (the so-called 'presenium') and 9 to 12 months in the mouse. Nevertheless, these models have served to elu cidate many of the pathways underlying the human disease processes, for instance clarifying the neuronal origin of parenchymal and perivascular amyloid in Alzheimer's disease and Creutzfeldt-Jakob disease. 212 pp. Englisch.

Condizione: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. The natural history of Alzheimer s Disease: minding the gaps in understanding the mechanisms of neurodegeneration.-Pathological mechanisms in Huntingdon s Disease and other polyglutamine expansion diseases.-Prion protein biogenesis: implications for neurode.

Condizione: New. Print on Demand pp. xiv + 190 28 Illus. (8 Col.).

Taschenbuch. Condizione: Neu. This item is printed on demand - Print on Demand Titel. Neuware -Fondation Ipsen sponsored a meeting in Paris in February 2000 on the emerging paradigm-shift in our understanding of the major degenerative diseases which affect the aging human brain. This book sumarizes our deliberations on some of these major neurodegenerative diseases that are characterized by protein depos its, and that are due to the pathogenic gain of function of an otherwise normal neuronal protein. For each of the major human neurodegenerative diseases covered in this book -the most prominent being Alzheimer's disease -experimental models are described, including cell culture systems and animal models which range from the round worm, Caenorhabditis elegans, the fruitfly, Drosophila melanogaster, to rodents. Remarkably, in the sporadic forms of these human diseases, only a minor change in the level of production or turn-over of the relevant proteins is sufficient to cause disease in late adult-hood. Neurodegeneration in Alzheimer's disease, for example, usually results in symptoms and signs in the seventh to eighth decades. In contrast, the development of protein deposits in transgenic mice over-expressing the corresponding disease gene parallels the genetic forms of the human diseases in regard to its manifestation occuring half-way through its normal life-span, i. e. about 50 years in humans (the so-called 'presenium') and 9 to 12 months in the mouse. Nevertheless, these models have served to elu cidate many of the pathways underlying the human disease processes, for instance clarifying the neuronal origin of parenchymal and perivascular amyloid in Alzheimer's disease and Creutzfeldt-Jakob disease.Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg 208 pp. Englisch.

Condizione: New. PRINT ON DEMAND pp. xiv + 190.