In human samples from patients with Alzheimer’s, the levels of the SFRP1 protein are abnormally high and increase as the disease progresses. Image: Pilar Esteve, CSIC
A new study carried out by researchers from the University of Barcelona, the Institute of Neurosciences of the UB (UBNeuro), the Institute of Neuropathology of the University Hospital Bellvitge-IDIBELL and the Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED) have identified a new therapeutical target to treat Alzheimer’s disease.
The new study states that, in human samples from patients with Alzheimer’s, the levels of the SFRP1 protein are abnormally high and increase as the disease progresses.
According to the conclusions of the study, the inactivation of the SFRP1 protein with specific bodies is able to inhibit the production of the β-amyloid protein –which accumulates in brain deposits in Alzheimer’s disease- and reduce the deposits of senile plaques in animal models.
“From a therapeutical perspective, the most important thing in the study is to check that the treatment led to an improvement in the cognitive deficits, the electrophysiological functioning and the nervous transmission in the studied mice”, notes Isidre Ferrer, professor at the Department of Pathology and Experimental Therapeutics of the UB and director of the Institute of Neuropathology at the University Hospital Bellvitge-IDIBELL.
The study was published in the journal Nature Neuroscience and was led by the doctors Paola Bovolenta and Pilar Esteve, from the Center for Molecular Biology Severo Ochoa and and the Rare Diseases Networking Biomedical Research Centre (CIBERER). Other experts have taken part in the research team: Isidre Ferrer, Ester Aso and Paula García-Esparcia, from the Faculty of Medicine and Health Sciences, UBNeuro and CIBERNED.
