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

Lluís Pujadas (), Daniela Rossi, Rosa Andrés, Cátia M. Teixeira, Bernat Serra-Vidal, Antoni Parcerisas, Rafael Maldonado, Ernest Giralt, Natàlia Carulla and Eduardo Soriano ()
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Lluís Pujadas: University of Barcelona
Daniela Rossi: University of Barcelona
Rosa Andrés: University of Barcelona
Cátia M. Teixeira: University of Barcelona
Bernat Serra-Vidal: Institute for Research in Biomedicine, Barcelona (IRB Barcelona)
Antoni Parcerisas: University of Barcelona
Rafael Maldonado: University Pompeu Fabra
Ernest Giralt: Institute for Research in Biomedicine, Barcelona (IRB Barcelona)
Natàlia Carulla: Institute for Research in Biomedicine, Barcelona (IRB Barcelona)
Eduardo Soriano: University of Barcelona

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms4443

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