Neurosciences

Neural Development, Regeneration & Neurodegeneration

Eduardo Soriano García

Research assistant Marco Antonio Solis | Research associates Ferran Burgaya,  Jesús Ureña, Marta Pascual, Alexander Fausto Ulloa, Lluis Pujadas, Tiziana Cotrufo | Researchers in training:
Daniela Rossi, Serena Mirra, Yasmina Manso, Jonatan Dorca, Mónica Pardo, Antoni Parcerisas, Cristina Roselló, Marc Hernaiz, Irene Lobon, Alba del Valle Vilchez | MSC and visiting students
Alva Ortega Gascó, Boris Bouazza Arostegui, Laura Llaó Cid, Laia Torres Masjoan, Sara Gregorio Jordan | Lab technician Ashraf Muhaisen

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Summary

Throughout this year we have focused mainly on two hypotheses regarding the pathogenesis of Alzheimer’s Disease (AD) and potential therapeutic strategies: 1) Reelin is an extracellular protein crucial for brain development, which is also expressed in the adult brain. Recent studies support the relationship between Reelin and AD and we have hypothesized that by regulating metabolism Aß42, phosphorylation of Tau and synaptic plasticity in adults, the Reelin cascade may be an important regulator of brain function and plasticity in adults. We tested the hypothesis that Reelin may be protective in AD by overexpression of Reelin (Reelin-OE mice) in a model of AD (J20). The Reelin-OE/J20 mice showed decreased plaque burden and rescue of synaptic and cognitive deficits, suggesting that Reelin protects from AD pathology. 2) Some human diseases (eg, cancer), are caused by somatic mutations that alter the function of specific cells. Through exome sequencing we have tested the hypothesis that somatic mutations are present in the brain of AD. We have found a remarkable number of specific SNVS. We believe these data reveal important new molecular and genetic information to understand the mechanisms that trigger the AD and open new therapeutic avenues.

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