Perfil
Jesús Avila is a Professor and former Director of the Center of Molecular Biology in Madrid, Spain and CIBERNED, Spain. Over the last forty years, he has dedicated his research to studying the neuronal cytoskeleton, focusing primarily on the tau protein’s role in neurodegenerative disorders, particularly tauopathies like Alzheimer’s disease.
Prof. Avila is an elected member of multiple prestigious organizations, including the European Molecular Biology Organization (EMBO), the American Association for the Advancement of Science (AAAS), the European Academy, the Academy of Sciences of Lisbon and the Spanish Royal Academies of Sciences and Medicine, among others. He serves on the editorial boards of several renowned journals and has authored over 600 scientific articles, most of which pertain to Alzheimer’s disease. His work has made significant contributions to understanding the mechanisms underlying neurodegeneration.
Prof. Avila’s research initially centered on the neuronal cytoskeleton, Alzheimer’s disease, and axonal regeneration. In recent years, his team has concentrated mainly on Alzheimer’s disease, a condition characterized by two hallmark pathological structures in the brain: Senile plaques, composed of beta-amyloid peptides and Neurofibrillary tangles, whose primary component is the tau protein. A potential link between beta-amyloid aggregates and tau protein aggregation involves the activation of the protein kinase GSK3 (glycogen synthase kinase 3). Prof. Avila’s team has developed and analyzed a transgenic mouse model overexpressing GSK3 in the brain, providing critical insights into its role in disease progression. The group’s recent efforts have focused on: a) Investigating the structure and function of tau in both physiological and pathological states b) Exploring the mechanisms of tau pathology spreading during Alzheimer’s progression c) Identifying novel neuronal functions of tau protein d) Developing strategies for reprogramming (or rejuvenating) cells in the dentate gyrus—a brain region essential for adult neurogenesis and severely affected in Alzheimer’s disease.
