• Open Access

Prion protein and Aβ-related synaptic toxicity impairment

Authors

  • Anna Maria Calella,

    1. Institute of Neuropathology, University Hospital Zürich, Zürich, Switzerland
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    • These authors contributed equally to this work.

  • Mélissa Farinelli,

    1. Medical Faculty of the University of Zürich, Department of Biology, Brain Research Institute, Swiss Federal Institute of Technology, Zürich, Switzerland
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    • These authors contributed equally to this work.

  • Mario Nuvolone,

    1. Institute of Neuropathology, University Hospital Zürich, Zürich, Switzerland
    2. Department of Internal Medicine, Amyloid Center, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy
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    • These authors contributed equally to this work.

  • Osvaldo Mirante,

    1. Medical Faculty of the University of Zürich, Department of Biology, Brain Research Institute, Swiss Federal Institute of Technology, Zürich, Switzerland
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  • Rita Moos,

    1. Institute of Neuropathology, University Hospital Zürich, Zürich, Switzerland
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  • Jeppe Falsig,

    1. Institute of Neuropathology, University Hospital Zürich, Zürich, Switzerland
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  • Isabelle M. Mansuy,

    Corresponding author
    1. Medical Faculty of the University of Zürich, Department of Biology, Brain Research Institute, Swiss Federal Institute of Technology, Zürich, Switzerland
    • Isabelle M. Mansuy, Tel: +41 44 635 33 60; Fax: +41 44 635 33 03

      Adriano Aguzzi, Tel: +41-44-255 2107; Fax: +41-44 255 44 02

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  • Adriano Aguzzi

    Corresponding author
    1. Institute of Neuropathology, University Hospital Zürich, Zürich, Switzerland
    • Isabelle M. Mansuy, Tel: +41 44 635 33 60; Fax: +41 44 635 33 03

      Adriano Aguzzi, Tel: +41-44-255 2107; Fax: +41-44 255 44 02

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Abstract

Alzheimer's disease (AD), the most common neurodegenerative disorder, goes along with extracellular amyloid-β (Aβ) deposits. The cognitive decline observed during AD progression correlates with damaged spines, dendrites and synapses in hippocampus and cortex. Numerous studies have shown that Aβ oligomers, both synthetic and derived from cultures and AD brains, potently impair synaptic structure and functions. The cellular prion protein (PrPC) was proposed to mediate this effect. We report that ablation or overexpression of PrPC had no effect on the impairment of hippocampal synaptic plasticity in a transgenic model of AD. These findings challenge the role of PrPC as a mediator of Aβ toxicity.

See accompanying article: http://dx.doi.org/10.1002/emmm.2010000868.

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