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06/03/2014

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

2014_0059_2014_0059_IMATGE

06/03/2014

The study is co-led by Dr. Eduardo Soriano, researcher with double appointment at VHIR and the UB

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 on the journal " "http://www.nature.com/ncomms/2014/140306/ncomms4443/full/ncomms4443.html" Nature Communications, co-led by Eduardo Soriano, researcher from Vall d'Hebron Institute of Research 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 is part of the PhD thesis developed by Daniela Rossi, co-author of the article together with Lluís Pujadas. Natàlia Carulla, from the Institute for Research in Biomedicine (IRB), collaborated actively in the research too. Other participants are: M. Rosa Andrés, Cátia M. Teixeira, Antoni Parcerisas, Ernest Giralt, Bernat Serra and Rafael Maldonado, and the institutions Research Center for Neurological Diseases Foundation (CIEN Foundation) and Pompeu Fabra University (UPF).To recover cognitive functions in models of Alzheimer’s diseaseAlzheimer’s disease is a neurodegenerative disease characterised by progressive cognitive deficits, synaptic loss and neuronal death. It is mainly associated with the formation of senile plaques (extracellular deposits of amyloid-ß, Aß) and the presence of neurofibrillary tangles (intracellular bundles of tau protein). The disease, which is the most common form of dementia in the elderly, affects more than 100,000 people in Catalonia and 500,000 in Spain, and causes progressive degeneration of patients’ intellectual and cognitive functions.This new preclinical study proves that an increase in Reelin brain levels avoids cognitive deterioration in mouse models of Alzheimer’s disease. Moreover, Reelin delays amyloid-beta fibril formation in vitro and reduces amyloid deposits in mice with Alzheimer’s.The double pathway of Aß peptide and tau proteinProfessor Eduardo Soriano, head of the Research Group Developmental Neurobiology and Neuroregeneration of UB, explains that “most studies on Alzheimer’s disease search for therapeutic targets addressed to a certain process involved in the disease”. On the contrary, “our study analyses the signalling pathway of Reelin—a synaptic and cognitive enhancer— that regulates the amyloid precursor protein (APP) and tau protein, which are both involved in basic processes of Alzheimer’s disease”.Lluís Pujadas, first author of the article together with Daniela Rossi, points out: “We knew that Reelin is involved in the double regulating pathway of Aß peptide and tau protein, but it was difficult to understand their interaction”. “The study —he adds—, shows a new mechanism that enables to understand better the link between both aspects of the disease”. The investigation describes how Reelin, trapped into amyloid fibrils, loses its ability to promote plasticity, thus, Reelin overexpression may be beneficial.

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