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Abstract

Alzheimer disease is accompanied by memory deficits. These deficits could be the consequence of changes in adult dentate gyrus neurogenesis. As a first step to analyze those changes we have used a transgenic mouse model that shows an impaired neurogenesis upon over expression of GSK3, a protein kinase that could be activated in Alzheimer disease (AD). Our results have indicated a deficient morphology in adult newborn neurons that are unable to connect properly with the preexisting neurons. These observations found in the mouse model were compared to the features found in the brain of Alzheimer disease patients and some similarities were found. Our results suggest that an impaired neurogenesis may be responsible of the memory deficits found in AD patients.

Biography

Jesus Avila is Professor and former Director of the Center of Molecular Biology Madrid, Spain. During the last thirty years he had been working in neuron cytoskeleton. Now he studies the role of tau protein in neurodegenerative disorders tauopathies like Alzheimer's disease. He is member of different Organizations like EMBO European Academy and the Spanish Royal Academy of Sciences; he is member of different Editorial Boards and has more than 300 publications most of them related with Alzheimer's disease.