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Dipòsit Digital de Documents de la UAB 3 registres trobats  La cerca s'ha fet en 0.00 segons. 
1.
52 p, 705.6 KB Role of Amyloid-β and Tau Proteins in Alzheimer's Disease : Confuting the Amyloid Cascade / Gulisano, W. (Department of Biomedical and Biotechnological Sciences. Section of Physiology. University of Catania) ; Maugeri, Daniele (Department of Biomedical and Biotechnological Sciences. Section of Physiology. University of Catania) ; Baltrons Soler, Ma. Antonia (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular) ; Fà, Mauro (Taub Institute for Research on Alzheimer's Disease and the Aging Brain. Department of Medicine. Columbia University) ; Amato, Arianna (Department of Anaesthesiology. Università Cattolica Del Sacro Cuore) ; Palmeri, Agostino (Department of Biomedical and Biotechnological Sciences. Section of Physiology. University of Catania) ; D'Adamio, Luciano (Department of Pharmacology. Physiology and Neuroscience. Rutgers University) ; Grassi, Claudio (Institute of Human Physiology. Università Cattolica Del Sacro Cuore) ; Devanand, D.P. (Department of Psychiatry. Columbia University. College of Phys. and Surg.) ; Honig, Lawrence S. (Department of Neurology. Columbia University. College of Phys. and Surg.) ; Puzzo, Daniela (Department of Biomedical and Biotechnological Sciences. Section of Physiology. University of Catania) ; Arancio, Ottavio (Taub Institute for Research on Alzheimer's Disease and the Aging Brain. Department of Medicine. Columbia University)
The "Amyloid Cascade Hypothesis" has dominated the Alzheimer's disease (AD) field in the last 25 years. It posits that the increase of amyloid-β (Aβ) is the key event in AD that triggers tau pathology followed by neuronal death and eventually, the disease. [...]
2018 - 10.3233/JAD-179935
Journal of Alzheimer's disease, Vol. 64 Núm. s1 (2018) , p. S611-S631  
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2.
15 p, 1.8 MB Extracellular Tau Oligomers Produce An Immediate Impairment of LTP and Memory / Fá, M. (Columbia University. Department of Pathology and Cell Biology) ; Puzzo, D. (University of Catania. Department of Biomedical and Biotechnological Sciences) ; Piacentini, R. (Università Cattolica del Sacro Cuore. Institute of Human Physiology) ; Staniszewski, A. (Columbia University. Department of Pathology) ; Zhang, H. (Columbia University. Department of Pathology) ; Baltrons Soler, Ma. Antonia (Universitat Autònoma de Barcelona. Institut de Biotecnologia i de Biomedicina "Vicent Villar Palasí") ; Li Puma, D. D. (Università Cattolica del Sacro Cuore. Institute of Human Physiology) ; Chatterjee, I. (Oligomerix) ; Li, J. (Third Military Medical University. Department of Neurology) ; Saeed, F. (Columbia University. Department of Pathology and Cell Biology) ; Berman, H. L. (Columbia University. Department of Pathology) ; Ripoli, C. (Università Cattolica del Sacro Cuore. Institute of Human Physiology) ; Gulisano, W. (University of Catania. Department of Biomedical and Biotechnological Sciences) ; Gonzalez, J. (Rockefeller University. Translational Technology Core Laboratory) ; Tian, H. (Tempe. Department of Chemical Engineering) ; Costa, J. A. (Columbia University. Department of Pathology and Cell Biology) ; Lopez, P. (Oligomerix) ; Davidowitz, E. (Oligomerix) ; Yu, W. H. (Columbia University. Department of Pathology and Cell Biology) ; Haroutunian, V. (The Mount Sinai School of Medicine. Department of Psychiatry) ; Brown, L. M. (Columbia University. Department of Biological Sciences) ; Palmeri, A. (University of Catania. Department of Biomedical and Biotechnological Sciences) ; Sigurdsson, E. M. (NYU Langone Medical Center. Department of Neuroscience and Physiology) ; Duff, K. E. (Columbia University. Department of Pathology and Cell Biology) ; Teich, A. F. (Columbia University. Department of Pathology and Cell Biology) ; Honig, L. S. (Columbia University. Department of Pathology and Cell Biology) ; Sierks, M. (Rockefeller University. Translational Technology Core Laboratory) ; Moe, J. G. (Oligomerix) ; D'Adamio, L. (Einstein College of Medicine. Department of Microbiology and Immunology) ; Grassi, C. (Hospitalization and Health Care) ; Kanaan, N. M. (College of Human Medicine. Department of Translational Science and Molecular Medicine) ; Fraser, P. E. (University of Toronto. Department of Medical Biophysics) ; Arancio, Ottavio (Columbia University. Department of Pathology and Cell Biology) ; Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular
Non-fibrillar soluble oligomeric forms of amyloid-β peptide (oAβ) and tau proteins are likely to play a major role in Alzheimer's disease (AD). The prevailing hypothesis on the disease etiopathogenesis is that oAβ initiates tau pathology that slowly spreads throughout the medial temporal cortex and neocortices independently of Aβ, eventually leading to memory loss. [...]
2016 - 10.1038/srep19393
Scientific reports, Vol. 6 (January 2016) , art. 19393  
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3.
19 p, 7.5 MB Reducing the Levels of Akt Activation by PDK1 Knock-in Mutation Protects Neuronal Cultures against Synthetic Amyloid-Beta Peptides / Yang, Shaobin (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Pascual-Guiral, Sònia (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Ponce, Rebeca (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Gimenez-Llort, Lydia (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Baltrons Soler, Ma. Antonia (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular) ; Arancio, Ottavio (Columbia University) ; Palacio Cornide, José Ramón (Universitat Autònoma de Barcelona. Departament de Biologia Cel·lular, de Fisiologia i d'Immunologia) ; Clos, Victòria (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Yuste, Victor J.. (Víctor José) (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Bayascas Ramírez, José Ramón (Universitat Autònoma de Barcelona. Institut de Neurociències)
The Akt kinase has been widely assumed for years as a key downstream effector of the PI3K signaling pathway in promoting neuronal survival. This notion was however challenged by the finding that neuronal survival responses were still preserved in mice with reduced Akt activity. [...]
2018 - 10.3389/fnagi.2017.00435
Frontiers in aging neuroscience, Vol. 9 (January 2018) , art. 435  
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