Jesus Avila & Jose J Lucas 
Animal Models for Neurodegenerative Disease [PDF ebook] 

Preface; Animal models on Alzheimer Disease; Animal models for Amyloid/PS-1 Pathology; Transgenic mice overexpressing GSK-3beta as animal models of Alzheimer Disease; Reelin and Alzheimer Disease; Tauopathy models; Animal models for Parkinson Disease I; Animal models for Parkinson Disease II; Neuroprotection in Parkinson Disease; Animal models for ALS; Mouse models of Huntington’s Disease; Recesive Ataxias; Mouse models in Pr P-related diseases; Mouse models of ischemia;

Jesus Avila is a Professor and former Director of the Centre of Molecular Biology in Madrid. Over the last thirty years, his work has focused on the cytoskeleton of the neuron. He is now investigating on the role of tau proteins in neurodegenerative disorders (tauopathies) such as Alzheimer’s disease. Professor Avila is a member of several professional organizations including EMBO, the European Academy, and the Spanish Royal Academy of Sciences. He is also on the Editorial Board of a number of scholarly journals and has more than 300 publications to his name. Jose J. Lucas is Research Professor of the Spanish National Research Council (CSIC) at the Centre for Molecular Biology (CBMSO) in Madrid. He obtained his Ph D from the Cajal Institute in 1993 and then moved to Columbia University in New York for his postdoctoral training. He subsequently returned to Spain to join CBMSO and, in recent years, his research has focused on the generation of mouse models to study neurodegeneration and other CNS diseases. Professor Lucas is a member of several professional organizations including the European Huntington’s Disease Network (EHDN) and the Spanish Royal Academy of Pharmacy. He has authored more than 70 papers including contributions on the potential for reversibility of neurodegenerative disorders. FÚlix Hernßndez lectures on Biochemistry and Molecular Biology at Autonoma University in Madrid. His main research focus is on neurodegenerative diseases, such as Alzheimer’s and related tauopathies, using genetically modified mouse models – especially those over-expressing mutated tau protein and its main kinase, GSK-3?.