M
Manuel Buttini
Researcher at University of California, San Francisco
Publications - 37
Citations - 4062
Manuel Buttini is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Apolipoprotein E & In situ hybridization. The author has an hindex of 22, co-authored 37 publications receiving 3922 citations. Previous affiliations of Manuel Buttini include Élan & Gladstone Institutes.
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Journal ArticleDOI
Neuron-Specific Apolipoprotein E4 Proteolysis Is Associated with Increased Tau Phosphorylation in Brains of Transgenic Mice
Walter J. Brecht,Faith M. Harris,Shengjun Chang,Ina Tesseur,Gui-Qiu Yu,Qin Xu,Jo Dee Fish,Tony Wyss-Coray,Manuel Buttini,Lennart Mucke,Robert W. Mahley,Yadong Huang +11 more
TL;DR: Neuron-specific proteolytic cleavage of apoE4 is associated with increased phosphorylation of tau and may play a key role in the development of AD-related neuronal deficits.
Journal ArticleDOI
Expression of human apolipoprotein E3 or E4 in the brains of Apoe-/- mice: isoform-specific effects on neurodegeneration.
Manuel Buttini,Matthias Orth,Stefano Bellosta,Hassibullah Akeefe,Robert E. Pitas,Robert E. Pitas,Tony Wyss-Coray,Lennart Mucke,Robert W. Mahley,Robert W. Mahley +9 more
TL;DR: Differences in the effects of apoE isoforms on neuronal integrity may relate to the increased risk of Alzheimer’s disease and to the poor outcome after head trauma and stroke associated with Apoe−/− mice in humans.
Journal ArticleDOI
Isoform-specific effects of human apolipoprotein E on brain function revealed in ApoE knockout mice: Increased susceptibility of females
Jacob Raber,Derek Wong,Manuel Buttini,Matthias Orth,Stefano Bellosta,Stefano Bellosta,Robert E. Pitas,Robert W. Mahley,Lennart Mucke +8 more
TL;DR: It is demonstrated that human apoE isoforms have differential effects on brain function in vivo and that the susceptibility to APOE epsilon4-induced deficits is critically influenced by age and gender.
Journal ArticleDOI
Partial Reduction of BACE1 Has Dramatic Effects on Alzheimer Plaque and Synaptic Pathology in APP Transgenic Mice
Lisa McConlogue,Manuel Buttini,John P. Anderson,Elizabeth F. Brigham,Karen S. Chen,Stephen B. Freedman,Dora Games,Kelly Johnson-Wood,Michael K. Lee,Michelle Zeller,Weiqun Liu,Ruth Motter,Sukanto Sinha +12 more
TL;DR: Quantitative analyses indicate that brain Aβ levels in young APP transgenic mice are not the sole determinant for the changes in plaque pathology mediated by reduced BACE1, and demonstrate that partial reductions of Bace1 enzyme activity and concomitant A β levels lead to dramatic inhibition of Aβ-driven AD-like pathology.
Journal ArticleDOI
RAGE potentiates Aβ-induced perturbation of neuronal function in transgenic mice
Ottavio Arancio,H. Zhang,Xi Chen,Chang Lin,Fabrizio Trinchese,Daniela Puzzo,Shumin Liu,Ashok N. Hegde,Shi Fang Yan,Alan Stern,John S. Luddy,Lih-Fen Lue,Douglas G. Walker,Alex E. Roher,Manuel Buttini,Lennart Mucke,Weiying Li,Ann Marie Schmidt,Mark S. Kindy,Mark S. Kindy,Paul A. Hyslop,David M. Stern,Shirley ShiDu Yan +22 more
TL;DR: It is indicated that RAGE is a cofactor for Aβ‐induced neuronal perturbation in a model of Alzheimer's‐type pathology, and its potential as a therapeutic target to ameliorate cellular dysfunction is suggested.