Jucker Mathias (44 results)

Hardcover. Condition: Very Good. No Jacket. Missing dust jacket; May have limited writing in cover pages. Pages are unmarked. ~ ThriftBooks: Read More, Spend Less.

Hardcover. Condition: Very Good. Hardcover, xxxiii + 543 pages, illustrated, NOT ex-library. A clean copy with unmarked text, free of inscriptions and stamps. Issued without a dust jacket. Contents: Alois Alzheimer [Concerning a unique disease of the cerebral cortex; History of Alzheimer's first case Auguste D; Alzheimer & beginnings of research into Alzheimer's disease; Alzheimer & the myth of the pioneer]; Beginning of modern research [Alzheimer's Disease at mid-Century; Alzheimer's disease research]; Anatomy & Neuropsychology [Anatomical changes underlying dementia in Alzheimer's disease; Staging of cortical neurofibrillary inclusions of the Alzheimer's type; Of stains & brains: how microscopic & clinical observations contributed to the understanding of Alzheimer's disease; Presenile forms of Alzheimer's disease in 2006]; Cholinergic Deficit [Acetylcholine in AD: Expectations meet reality]; Amyloid & Genetics [Discovery of [Beta] Amyloid; Pathways to the discovery of the neuronal origin & proteolytic biogenesis of A[Beta] amyloid of Alzheimer's disease; Amyloid Hypothesis: history & alternatives; Segregation of a missense mutation in the amyloid [Beta]-protein precursor gene with familial Alzheimer's disease; From the amyloid [Beta] protein (A4) to isolation of the first Alzheimer's disease gene: amyloid [Beta] (A4) precursor protein (APP); Commentary on "Correlative memory deficits, A[Beta] elevation & amyloid plaques in transgenic mice"; Vision for the future: pathogenesis, models & experimental therapeutics; PS1, PS2 & APP mutations that cause Alzheimer's disease increase A[Beta]42; Amyloid precursor protein, AD & Down's syndrome; Catabolism of amyloid [Beta] peptide & pathogenesis of sporadic Alzheimer's disease; Synaptic activity, amyloid-[Beta] & AD; Molecular pathogenesis of AD in human peripheral cells: platelets show it all; Neuronal origin hypothesis of cerebral amyloid angiopathy; Neuropathologist & Alzheimer genetics; Genetics, molecular biology & animal modeling of AD; Genetic Alzheimer-frontotemporal dementia spectrum; Mutation of the AD amyloid gene in hereditary cerebral hemorrhage, Dutch type; Physiological generation of Amyloid [Beta]-peptide & its Consequences for AD Research; Activation of [Alpha]-secretase as an approach for treatment of AD; Challenges to the enigma of [gamma]-secretase & to AD; Targeting [gamma]-Secretase; Presenilin/gamma-secretase complex & its potential as a drug target; Identification of [Beta]-secretase]; ApoE [Apolipoprotein E & AD; Apolipoprotein E4: From synaptic remodeling to genetic risk factor in both familial & sporadic AD]; Tau [Alzheimer tangle: 100 years on; Immunological demonstration of tau protein in nearofibrillary tangles; Bulk isolation of neurofibrillary tangles & discoveries of tau & its abnormal hyperphosphorylation; Natural & molecular history of AD; Tau focused drug discovery for AD & related Neurodegenerative Tauopathies; Ubiquitin is a component of paired helical filaments; Influence of tau on neuronal traffic mechanisms; Search for structure of tau & paired helical filaments]; Oxidative Stress [Changing landscape of AD: From Insoluble to Soluble & from Pathogen to Protector; Molecular & cellular pathways towards and away from AD]; Epidemiology [Paquid]; Imaging [Hippocampal imaging in the early diagnosis of AD 1988 to 2006; Detecting Early-Stage AD in MCI & PreMCI; Imaging the pathology of AD: Building on a century-Old blueprint]; Therapeutical Perspectives [How do we test drugs; Inflammation & lesions of AD; A[Beta] immunotherapy prevents & Reverses AD neuropathology; Immunotherapy; "Magic" bullets, shotguns or cocktails to treat or prevent AD?; Seventh age of man: Solving senility]; Forum & Network [Fondation Ipsen & AD: a 20-year relationship; Alzheimer Research Forum: A Knowledge Base and e-Community for AD Research; Potamkin prize for research in Pick's, Alzheimer's and related diseases]; Subject Index.

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Hardcover. Condition: Very Good. Hardcover (no jacket) in very good condition. One or two slight bumps and signs of wear to the board edges. A few light marks on the page block. Pages are clean; all text and colour images are clear. CM. Used.

Hardcover. Condition: Bon. Ancien livre de bibliothèque avec équipements. Edition 2006. Ammareal reverse jusqu'à 15% du prix net de cet article à des organisations caritatives. ENGLISH DESCRIPTION Book Condition: Used, Good. Former library book. Edition 2006. Ammareal gives back up to 15% of this item's net price to charity organizations.

Hardcover. Condition: Very good. Hardcover Octavo no dust jacket. illustrated boards, white lettering, no dust jacket, 543 pp.

Relié. Condition: D'occasion - Comme neuf. === ENVOIE LE JOUR MEME ===.

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Condition: New.

Taschenbuch. Condition: Neu. Druck auf Anfrage Neuware - Printed after ordering - 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.

Buch. Condition: Neu. Druck auf Anfrage Neuware - Printed after ordering - 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.

Buch. Condition: Neu. Neuware -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. ¿Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg 168 pp. Englisch.

Hardcover. Condition: Brand New. 2013 edition. 175 pages. 9.25x6.25x0.50 inches. In Stock.

Paperback. Condition: Brand New. 2013 edition. 168 pages. 9.25x6.10x0.38 inches. In Stock.

Condition: New. In.

Hardcover. Condition: Like New. LIKE NEW. SHIPS FROM MULTIPLE LOCATIONS. book.

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Gebunden. Condition: New.

Condition: New. pp. 580.

Condition: New. pp. 580.

Condition: New. pp. 580.

Taschenbuch. Condition: Neu. Druck auf Anfrage Neuware - Printed after ordering - Few medical or scientific addresses have so unmistakeably made history as the presentation delivered by Alois Alzheimer on November 4, 1906 in Tübingen. The celebratory event, 'Alzheimer 100 Years and Beyond' organized on the initiation of the Alzheimer community in Germany and worldwide, in collaboration with the Fondation Ipsen, was the highlight of the Year of Alzheimer. However, beyond these few months of tributes, the centennial offers a unique opportunity to assess both the progress achieved and the uncertainties remaining. This volume, a collection comprised mainly of articles by the invited speakers and also of a few other prominent researchers, is meant to be a record of those events.

Buch. Condition: Neu. Druck auf Anfrage Neuware - Printed after ordering - Few medical or scientific addresses have so unmistakeably made history as the presentation delivered by Alois Alzheimer on November 4, 1906 in Tübingen. The celebratory event, 'Alzheimer 100 Years and Beyond' organized on the initiation of the Alzheimer community in Germany and worldwide, in collaboration with the Fondation Ipsen, was the highlight of the Year of Alzheimer. However, beyond these few months of tributes, the centennial offers a unique opportunity to assess both the progress achieved and the uncertainties remaining. This volume, a collection comprised mainly of articles by the invited speakers and also of a few other prominent researchers, is meant to be a record of those events.

Taschenbuch. Condition: Neu. Neuware -Few medical or scientific addresses have so unmistakeably made history as the presentation delivered by Alois Alzheimer on November 4, 1906 in Tübingen.The celebratory event, 'Alzheimer 100 Years and Beyond' organized on the initiation of the Alzheimer community in Germany and worldwide, in collaboration with the Fondation Ipsen, was the highlight of the Year of Alzheimer. However, beyond these few months of tributes, the centennial offers a unique opportunity to assess both the progress achieved and the uncertainties remaining. This volume, a collection comprised mainly of articles by the invited speakers and also of a few other prominent researchers, is meant to be a record of those events.Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg 580 pp. Englisch.

Buch. Condition: Neu. Neuware -Few medical or scientific addresses have so unmistakeably made history as the presentation delivered by Alois Alzheimer on November 4, 1906 in Tübingen.The celebratory event, 'Alzheimer 100 Years and Beyond' organized on the initiation of the Alzheimer community in Germany and worldwide, in collaboration with the Fondation Ipsen, was the highlight of the Year of Alzheimer. However, beyond these few months of tributes, the centennial offers a unique opportunity to assess both the progress achieved and the uncertainties remaining. This volume, a collection comprised mainly of articles by the invited speakers and also of a few other prominent researchers, is meant to be a record of those events.Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg 580 pp. Englisch.

Hardcover. Condition: Like New. Like New. book.

Hardcover. Condition: Brand New. 1st edition. 543 pages. 9.25x6.25x0.75 inches. In Stock.