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Aβ-Induced Toxicity Mediated by Caspase Cleavage of the Amyloid Precursor Protein (APP)

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Synaptic Plasticity and the Mechanism of Alzheimer's Disease

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

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Abstract

Synapse and neuron losses are characteristic features ofAlzheimer’s disease (AD) and are believed to underlie the cognitive impairments seen in this disorder. Amyloid β-protein (Aβ) is hypothesized to play a pivotal role in initiating AD pathogenesis, but the precise mechanisms of Aβ-induced damage remain unclear. Caspases, a family of proteases best known for their role in programmed cell death, may play a role in neurodegeneration. This review will focus on recent findings implicating a role for caspase cleavage of the amyloid precursor protein (APP) in synaptic and neuronal injury in AD and how this pathway may be initiated by the interaction of Aβ with APP.

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Authors and Affiliations

  1. Department of Neurosciences, University of California, 92037, San Diego, CA, USA

    Edward H. Koo

  2. Buck Institute for Age Research, Novato, CA 94945 and Department of Neurology, University of California, 94143, San Francisco , CA, USA

    Dale E. Bredesen

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  1. Edward H. Koo
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  2. Dale E. Bredesen
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Editor information

Editors and Affiliations

  1. Center for Neurologic Diseases, Brigham andWomen’s Ho, Harvard Medical School, 02115, Boston, MA, USA

    Dennis J. Selkoe

  2. Laboratoire de Biologie Cellulaire de la Synapse, Institut National de la Santé et de la Recherche, Médicale Unite 789, 46 rue d’Ulm, 75005, Paris, France

    Antoine Triller

  3. Pour la Recherche Thérapeutique, Fondation IPSEN, 24, rue Erlanger, 75781, Paris Cedex 16, France

    Yves Christen

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© 2008 Springer-Verlag Berlin Heidelberg

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Koo, E., Bredesen, D. (2008). Aβ-Induced Toxicity Mediated by Caspase Cleavage of the Amyloid Precursor Protein (APP). In: Selkoe, D., Triller, A., Christen, Y. (eds) Synaptic Plasticity and the Mechanism of Alzheimer's Disease. Research and Perspectives in Alzheimer's Disease. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-76330-7_11

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