© 2008

Synaptic Plasticity and the Mechanism of Alzheimer's Disease

  • Dennis J. Selkoe
  • Antoine Triller
  • Yves Christen

Part of the Research and Perspectives in Alzheimer's Disease book series (ALZHEIMER)

Table of contents

  1. Front Matter
    Pages I-XII
  2. Marianne Renner, Antoine Triller
    Pages 1-18
  3. Antony Holtmaat, V. De Paola, L. Wilbrecht, G. Knott
    Pages 37-49
  4. Roberto Malinow, Helen Hsieh, Wei Wei
    Pages 63-68
  5. Veronica A. Alvarez, Ganesh M. Shankar, Brenda L. Bloodgood, Dennis J. Selkoe, Bernardo L. Sabatini
    Pages 75-87
  6. WilliamL. Klein, Fernanda De Felice, Pascale N. Lacor, Mary P. Lambert, Wei-Qin Zhao
    Pages 103-132
  7. John R. Cirrito, Floy R. Stewart, Steven Mennerick, David M. Holtzman
    Pages 133-143
  8. Michael J. Rowan, Igor Klyubin, William K. Cullen, NengWei Hu, Roger Anwyl
    Pages 157-167
  9. Thomas Bourgeron
    Pages 169-179
  10. Back Matter
    Pages 181-183

About this book


During most of the 20th century, neurodegenerative diseases remained among the most enigmatic disorders of medicine. The scientific study of these conditions was descriptive in nature, detailing the clinical and neuropathological phenotypes associated with various diseases, but etiologies and pathogenic mechanisms remained obscure. Beginning in the 1970s, advances in two principal areas – biochemical pathology and molecular genetics – combined to yield powerful clues to the molecular underpinnings of several previously "idiopathic" brain disorders. Among the classical neurodegenerative diseases, perhaps the most rapid progress occurred in research on Alzheimer’s disease (AD). In disorders like Huntington’s disease, amyotrophic lateral sclerosis and even Parkinson’s disease, unbiased genetic screens, linkage analysis and positional cloning have identified causative genes that subsequently allowed the formulation of specific biochemical hypotheses. In sharp contrast, modern research on AD developed in the opposite order: the identification of the protein subunits of the classical brain lesions guided geneticists to disease-inducing genes, for example, APP, apolipoprotein E and tau. Thus, a biochemical hypothesis of disease - that AD is a progressive cerebral amyloidosis caused by the aggregation of the amyloid b-protein (Ab) - preceded and enabled the discovery of etiologies.


Alzheimer Parkinson alzheimer's disease amyloid precursor protein attention deficit disorder (ADD) autism autism spectrum disorder brain cortex glutamate receptor memory postsynaptic density receptor receptor trafficking synapse loss

Editors and affiliations

  • Dennis J. Selkoe
    • 1
  • Antoine Triller
    • 2
  • Yves Christen
    • 3
  1. 1.Center for Neurologic Diseases, Brigham andWomen’s HoHarvard Medical SchoolBostonUSA
  2. 2.Laboratoire de Biologie Cellulaire de la Synapse, Institut National de la Santé et de la RechercheMédicale Unite 789ParisFrance
  3. 3.Pour la Recherche ThérapeutiqueFondation IPSENParis Cedex 16France

Bibliographic information

  • Book Title Synaptic Plasticity and the Mechanism of Alzheimer's Disease
  • Editors Dennis J. Selkoe
    Antoine Triller
  • Series Title Research and Perspectives in Alzheimer's Disease
  • DOI
  • Copyright Information Springer-Verlag 2008
  • Publisher Name Springer, Berlin, Heidelberg
  • eBook Packages Biomedical and Life Sciences Biomedical and Life Sciences (R0)
  • Hardcover ISBN 978-3-540-76329-1
  • Softcover ISBN 978-3-642-09519-1
  • eBook ISBN 978-3-540-76330-7
  • Series ISSN 0945-6066
  • Edition Number 1
  • Number of Pages XII, 183
  • Number of Illustrations 8 b/w illustrations, 26 illustrations in colour
  • Topics Neurosciences
    Human Physiology
  • Buy this book on publisher's site
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