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A study discovers that Reelin protein rescues cognitive deficits in an animal model of Alzheimer’s disease

By 6 de March de 2014November 18th, 2020No Comments
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From left to right, Daniela Rossi, Lluís Pujadas, Eduardo Soriano and Natàlia Carulla. Photo: UB.
 06.03.2014

A study discovers that Reelin protein rescues cognitive deficits in an animal model of Alzheimer’s disease

Reelin, a crucial protein for adult brain plasticity, recovers cognitive functions in mice with Alzheimer's disease. This is one of the main results of an article published today on the journal Nature Communications (doi:10.1038/ncomms4443), co-led by Eduardo Soriano, professor from the Department of Cell Biology at the University of Barcelona (UB) and member of the Centre for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), and researcher Lluís Pujadas (UB and CIBERNED). The study, which was started four years ago, has involved the collaboration of members of the Peptides and Proteins lab at the Institute for Research in Biomedicine (IRB), namely Bernat Serra-Vidal, PhD student, Ernest Giralt, group leader, and Natàlia Carulla, associate researcher.


Alzheimer’s disease, which affects approximately 500,000 people in Spain, is characterised by the loss of neural connections and by neuronal death, both associated mainly with the formation of senile plaques (extracellular deposits of Aβ) and the presence of neurofibrillary tangles (intracellular deposits of tau protein.

The study demonstrates how an increase in the levels of reelin—a protein that is essential for cerebral cortex plasticity—has the capacity to restore cognitive capacity in mouse models of Alzheimer’s disease, delaying amyloid-beta (Αβ) fibril formation in vitro and reducing the accumulation of amyloid deposits in the brains of animals affected by this disease.

In the IRB lab, researchers have performed experiments in vitro to determine whether there is an interaction between Aβ aggregation and reelin. These assays have revealed that reelin interacts with the Aβ peptide, delaying the formation of Aβ fibrils until it is trapped within them. “When reelins becomes trapped in Aβ fibrils, it loses its capacity to strengthen synaptic plasticity. This explains why an increase in reelin expression in the brain may be beneficial,” explain the authors of the study.

The hypotheses from the work in vitro have been tested in vivo using experimental animals. This study is the first to demonstrate a neuroprotective effect of reelin in neurodegenerative disease and, in addition, offers a possible explanation for this protective role.

The study has also involved scientists from the CIEN Foundation, the Vall d’Hebron Institut de Recerca (VHIR) and the University Pompeu Fabra (UPF). It forms part of the doctoral thesis of Daniela Rossi (UB and CIBERNED), principal co-author of the paper together with Lluís Pujadas.

More information on the on the website of the IRB [+] and on the UB [+] website.