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  • 1
    Online Resource
    Online Resource
    Abeta Peptide and Alzheimer’s Disease : Celebrating a Century of Research (2007)
    London : Springer-Verlag London Limited
    Details Availability
    Keywords: Medicine ; Human genetics ; Neurosciences ; Biochemistry ; Neurology ; Neurosurgery ; Medicine & Public Health ; Biochemistry ; Human genetics ; Medicine ; Neurology ; Neurosciences ; Neurosurgery ; Alzheimer Disease metabolism ; Alzheimer Disease etiology ; Amyloid beta-Protein metabolism ; Amyloid beta-protein ; Alzheimer's disease Molecular aspects ; Alzheimerkrankheit
    Description / Table of Contents: Recent advances in genetics and brain biochemistry point to the Abeta peptide as the major culprit in causing neurodegeneration in Alzheimer's Disease (AD). This book summarizes current knowledge of the Abeta peptide and its role in AD. Written by specialists in this fast moving area, the book covers fundamental biochemical studies on this peptide, the genetic impact on Abeta expression and processing, and various AD therapeutic strategies that target Abeta.
    Type of Medium: Online Resource
    Pages: Online-Ressource (XI, 298 p, digital)
    ISBN: 9781846284403
    Series Statement: SpringerLink
    URL: https://doi.org/10.1007/978-1-84628-440-3
    URL: http://dx.doi.org/10.1007/978-1-84628-440-3
    URL: https://swbplus.bsz-bw.de/bsz262064537cov.jpg
    URL: https://swbplus.bsz-bw.de/bsz262064537vor.htm
    URL: http://www.gbv.de/dms/bowker/toc/9781852339616.pdf
    DOI: 10.1007/978-1-84628-440-3
    RVK:
    YG 4000
    Language: English
    Note: Includes bibliographical references and index , Preface; CONTENTS; Contributors; 1 A Brief Introduction to the History of the ß-Amyloid Protein (Aß) of Alzheimer's Disease; 2. The Aßcentric Pathway of Alzheimer's Disease; 3. The Function of the Amyloid Precursor Protein Family; 4. The Involvement of Aß in the Neuroinflammatory Response; 5. Amyloid ß-Peptide(1-42), Oxidative Stress, and Alzheimer's Disease; 6. Amyloid Toxicity, Synaptic Dysfunction, and the Biochemistry of Neurodegeneration in Alzheimer's Disease; 7. Aß Variants and Their Impact on Amyloid Formation and Alzheimer's Disease Progression , 8. Copper Coordination by ß-Amyloid and the Neuropathology of Alzheimer's Disease9. Cholesterol and Alzheimer's Disease; 10. Amyloid ß-Peptide and Central Cholinergic Neurons: Involvement in Normal Brain Function and Alzheimer's Disease Pathology; 11. Physiologic and Neurotoxic Properties of Aß Peptides; 12. Impact of ß-Amyloid on the Tau Pathology in Tau Transgenic Mouse and Tissue Culture Models; 13. Glial Cells and Aß Peptides in Alzheimer's Disease Pathogenesis; 14. The Role of Presenilins in Aß-Induced Cell Death in Alzheimer's Disease , 15. Immunotherapeutic Approaches to Alzheimer's Disease16. Mouse Models of Alzheimer's Disease; Subject Index; Author Index
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  • 2
    Electronic Resource
    Electronic Resource
    The Role of the Amyloid Protein Precursor (APP) in Alzheimer's Disease: Does the Normal Function of APP Explain the Topography of Neurodegeneration? (1998)
    Springer
    Neurochemical research 23 (1998), S. 795-806 
    Details
    ISSN: 1573-6903
    Keywords: Alzheimer ; dementia ; amyloid ; neurite ; proteoglycan ; plaque
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alzheimer's disease (AD) is the most common form of dementia in the aged population. Early-onset familial AD (FAD) involves mutations in a gene on chromosome 21 encoding the amyloid protein precursor or on chromosomes 14 or 1 encoding genes known as presenilins. All mutations examined have been found to increase the production of amyloidogenic forms of the amyloid protein (Aβ), a 4 kDa peptide derived from APP. Despite the remarkable progress in elucidating the biochemical mechanisms responsible for AD, little is known about the normal function of APP. A model of how APP and Aβ are involved in pathogenesis is presented. This model may explain why certain neuronal populations are selectively vulnerable in AD. It is suggested that those neurons which more readily undergo neuritic sprouting and synaptic remodelling are more vulnerable to Aβ neurotoxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1022471729291
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