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Bernardo L. Sabatini
Researcher at Howard Hughes Medical Institute
Publications - 232
Citations - 29674
Bernardo L. Sabatini is an academic researcher from Howard Hughes Medical Institute. The author has contributed to research in topics: Dendritic spine & Postsynaptic potential. The author has an hindex of 77, co-authored 214 publications receiving 25610 citations. Previous affiliations of Bernardo L. Sabatini include University College London & Broad Institute.
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Journal ArticleDOI
Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory.
Ganesh M. Shankar,Shaomin Li,Tapan Mehta,Amaya Garcia-Munoz,Nina E. Shepardson,Imelda M. Smith,Francesca Brett,Michael A. Farrell,Michael J. Rowan,Cynthia A. Lemere,Ciaran M. Regan,Dominic M. Walsh,Bernardo L. Sabatini,Dennis J. Selkoe +13 more
TL;DR: It is concluded that soluble Aβ oligomers extracted from Alzheimer's disease brains potently impair synapse structure and function and that dimers are the smallest synaptotoxic species.
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Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway
Ganesh M. Shankar,Brenda L. Bloodgood,Matthew Townsend,Dominic M. Walsh,Dennis J. Selkoe,Bernardo L. Sabatini +5 more
TL;DR: It is concluded that soluble, low-n oligomers of human Aβ trigger synapse loss that can be reversed by therapeutic agents and provides a quantitative cellular model for elucidating the molecular basis of Aβ-induced neuronal dysfunction.
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ScanImage: Flexible software for operating laser scanning microscopes
Thomas A. Pologruto,Thomas A. Pologruto,Bernardo L. Sabatini,Bernardo L. Sabatini,Karel Svoboda +4 more
TL;DR: This work describes a simple, software-based approach to operating a laser scanning microscope without the need for custom data acquisition hardware and quantifies the effectiveness of the data acquisition and signal conditioning algorithm under a variety of conditions.
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Structure and function of dendritic spines.
TL;DR: Studies of compartmentalization have shown that spines serve primarily as biochemical, rather than electrical, compartments for rapid large-amplitude Ca(2+) signals underlying the induction of synaptic plasticity.
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The Life Cycle of Ca2+ Ions in Dendritic Spines
TL;DR: The kinetics of Ca(2+) sources governs the time course of [Ca(2+)] signals and may explain the selective activation of long-term synaptic potentiation (LTP) and long- term depression (LTD) by NMDA-R-mediated synaptic Ca( 2+).