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Reelin delays amyloid-beta fibril formation and rescues cognitive deficits in a model of Alzheimer’s disease

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  • Lluís Pujadas

    (University of Barcelona
    Centro de Investigación en Red sobre Enfermedades Neurodegenerativas (CIBERNED)
    Institute for Research in Biomedicine, Barcelona (IRB Barcelona)
    Vall D'Hebrón Institut de Recerca (VHIR))

  • Daniela Rossi

    (University of Barcelona
    Centro de Investigación en Red sobre Enfermedades Neurodegenerativas (CIBERNED)
    Institute for Research in Biomedicine, Barcelona (IRB Barcelona))

  • Rosa Andrés

    (University of Barcelona
    Centro de Investigación en Red sobre Enfermedades Neurodegenerativas (CIBERNED)
    Institute for Research in Biomedicine, Barcelona (IRB Barcelona))

  • Cátia M. Teixeira

    (University of Barcelona
    Centro de Investigación en Red sobre Enfermedades Neurodegenerativas (CIBERNED)
    Institute for Research in Biomedicine, Barcelona (IRB Barcelona))

  • Bernat Serra-Vidal

    (Institute for Research in Biomedicine, Barcelona (IRB Barcelona))

  • Antoni Parcerisas

    (University of Barcelona
    Centro de Investigación en Red sobre Enfermedades Neurodegenerativas (CIBERNED)
    Institute for Research in Biomedicine, Barcelona (IRB Barcelona)
    CIEN Foundation)

  • Rafael Maldonado

    (University Pompeu Fabra)

  • Ernest Giralt

    (Institute for Research in Biomedicine, Barcelona (IRB Barcelona)
    University of Barcelona)

  • Natàlia Carulla

    (Institute for Research in Biomedicine, Barcelona (IRB Barcelona))

  • Eduardo Soriano

    (University of Barcelona
    Centro de Investigación en Red sobre Enfermedades Neurodegenerativas (CIBERNED)
    Institute for Research in Biomedicine, Barcelona (IRB Barcelona)
    Vall D'Hebrón Institut de Recerca (VHIR))

Abstract

Reelin is an extracellular matrix protein that is crucial for neural development and adult brain plasticity. While the Reelin signalling cascade has been reported to be associated with Alzheimer’s disease (AD), the role of Reelin in this pathology is not understood. Here we use an in vitro approach to show that Reelin interacts with amyloid-β (Aβ42) soluble species, delays Aβ42 fibril formation and is recruited into amyloid fibrils. Furthermore, Reelin protects against both the neuronal death and dendritic spine loss induced by Aβ42 oligomers. In mice carrying the APPSwe/Ind mutation (J20 mice), Reelin overexpression delays amyloid plaque formation and rescues the recognition memory deficits. Our results indicate that by interacting with Aβ42 soluble species, delaying Aβ plaque formation, protecting against neuronal death and dendritic spine loss and preventing AD cognitive deficits, the Reelin pathway deserves consideration as a therapeutic target for the treatment of AD pathogenesis.

Suggested Citation

  • Lluís Pujadas & Daniela Rossi & Rosa Andrés & Cátia M. Teixeira & Bernat Serra-Vidal & Antoni Parcerisas & Rafael Maldonado & Ernest Giralt & Natàlia Carulla & Eduardo Soriano, 2014. "Reelin delays amyloid-beta fibril formation and rescues cognitive deficits in a model of Alzheimer’s disease," Nature Communications, Nature, vol. 5(1), pages 1-11, May.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4443
    DOI: 10.1038/ncomms4443
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