Advances in Alzheimer Disease Therapy

Alzheimer Disease

Therapeutic Strategies

Editors: Giacobini, E., Becker, R.E., Smith, D.L., Barton, J.M. (Eds.)

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About this book

Since the apoE4 allele is a risk factor or susceptibility gene in late-onset familial and sporadic AD, the mechanism of disease expression may involve metabolic effects that are isoform specific. Isoform-specific interactions of apoE therefore become critical in the mechanism of AD pathogenesis. Detailed characterization of the binding of the apoE isoforms with proteins and peptides relevant to the pathology of the disease may be critical in understanding disease pathogenesis. These critical isoform-specific interactions of apoE may involve interactions with proteins and pep tides in the defining neuropathologic lesions of the disease, the neurofibrillary tangle and senile plaque. Other possible critical isoform-specific interactions include the mechanism of internalization, intracellular trafficking, and subsequent metabolism. In addition, differential post-translational modifications of apoE isoforms may determine differences in metabolism contributing to the pathogenesis of the disease. Oxidation of apoE may confer several isoform-specific, biochemically distinct properties. Since {3A peptide binds apoE in the lipoprotein binding domain of the protein and not in the receptor-binding domain, apoE could target bound {3A4 peptide to neurons via the LRP receptor. Internalization of the apoEI {3A peptide complex into the cell, by the same route as the apoE-containing lipoproteins, would result in incorporation into primary lysosomes and pH dependent dissociation. The demonstration of apoE in the cytoplasm of neurons, with isoform-specific interactions of apoE with the microtubule-binding protein tau demonstrated in vitro, suggest additional, testable hypotheses of disease pathogenesis.

Table of contents (81 chapters)

  • Development of Drugs for Alzheimer Therapy: A Decade of Progress

    Giacobini, Ezio (et al.)

    Pages 1-7

  • Epidemiology of AD: Impact on the Treatment

    Amaducci, Luigi (et al.)

    Pages 8-13

  • Neuropathological Bases of Alzheimer Disease, Implications for Treatment

    Wisniewski, Henryk M. (et al.)

    Pages 17-22

  • Amyloid Deposition as the Central Event in the Etiology and Pathogenesis of Alzheimer’s Disease

    Hardy, John (et al.)

    Pages 23-27

  • Role of Abnormal Phosphorylation of Tau in Neurofibrillary Degeneration: Implications for Alzheimer Therapy

    Iqbal, Khalid (et al.)

    Pages 28-33

Buy this book

eBook $89.00
price for USA (gross)
  • ISBN 978-1-4615-8149-9
  • Digitally watermarked, DRM-free
  • Included format: PDF
  • ebooks can be used on all reading devices
  • Immediate eBook download after purchase
Softcover $119.00
price for USA
  • ISBN 978-1-4615-8151-2
  • Free shipping for individuals worldwide
  • Usually dispatched within 3 to 5 business days.
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Bibliographic Information

Bibliographic Information
Book Title
Alzheimer Disease
Book Subtitle
Therapeutic Strategies
Editors
  • D.L. Smith
  • J.M. Barton
  • Ezio Giacobini
  • Robert E. Becker
Series Title
Advances in Alzheimer Disease Therapy
Copyright
1994
Publisher
Birkhäuser Basel
Copyright Holder
Springer Science+Business Media New York
eBook ISBN
978-1-4615-8149-9
DOI
10.1007/978-1-4615-8149-9
Softcover ISBN
978-1-4615-8151-2
Edition Number
1
Number of Pages
XVI, 510
Number of Illustrations and Tables
27 b/w illustrations, 2 illustrations in colour
Topics