R
Robert E. Schmidt
Researcher at Washington University in St. Louis
Publications - 241
Citations - 14575
Robert E. Schmidt is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Sympathetic nervous system & Diabetic Autonomic Neuropathy. The author has an hindex of 58, co-authored 215 publications receiving 13327 citations. Previous affiliations of Robert E. Schmidt include Indiana University & Elsevier.
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Journal ArticleDOI
Inhibitors of protein synthesis and RNA synthesis prevent neuronal death caused by nerve growth factor deprivation.
David P. Martin,Robert E. Schmidt,P S DiStefano,Oliver H. Lowry,Joyce G. Carter,Eugene M. Johnson +5 more
TL;DR: The fact that sympathetic neurons must synthesize protein and RNA to die when deprived of NGF indicates that NGF, and presumably other neurotrophic factors, maintains neuronal survival by suppressing an endogenous, active death program.
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PGC-1alpha deficiency causes multi-system energy metabolic derangements: muscle dysfunction, abnormal weight control and hepatic steatosis.
Teresa C. Leone,John J. Lehman,Brian N. Finck,Paul J. Schaeffer,Adam R. Wende,Sihem Boudina,Michael Courtois,David F. Wozniak,Nandakumar Sambandam,Carlos Bernal-Mizrachi,Zhouji Chen,John O. Holloszy,Denis M. Medeiros,Robert E. Schmidt,Jeffrey E. Saffitz,E. Dale Abel,Clay F. Semenkovich,Daniel P. Kelly +17 more
TL;DR: It is demonstrated that PGC-1α is necessary for appropriate adaptation to the metabolic and physiologic stressors of postnatal life.
Journal ArticleDOI
IFN-stimulated gene 15 functions as a critical antiviral molecule against influenza, herpes, and Sindbis viruses.
Deborah J. Lenschow,Caroline Lai,Natalia Frias-Staheli,Nadia V. Giannakopoulos,Andrew Lutz,Thorsten Wolff,Anna Osiak,Beth Levine,Robert E. Schmidt,Adolfo García-Sastre,David A. Leib,Andrew Pekosz,Klaus Peter Knobeloch,Ivan Horak,Herbert W. Virgin +14 more
TL;DR: The demonstration of ISG15 as a novel antiviral molecule with activity against both RNA and DNA viruses provides a target for the development of therapies against important human pathogens.
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A complement–microglial axis drives synapse loss during virus-induced memory impairment
Michael J. Vasek,Charise Garber,Denise A. Dorsey,Douglas M. Durrant,Douglas M. Durrant,Bryan Bollman,Allison Soung,Jinsheng Yu,Carlos J. Perez-Torres,Arnaud Frouin,Daniel K. Wilton,Kristen E. Funk,Bette K. DeMasters,Xiaoping Jiang,James R. Bowen,Steven Mennerick,John K. Robinson,Joel R. Garbow,Kenneth L. Tyler,Mehul S. Suthar,Robert E. Schmidt,Beth Stevens,Robyn S. Klein +22 more
TL;DR: It is shown that viral infection of adult hippocampal neurons induces complement-mediated elimination of presynaptic terminals in a murine WNV neuroinvasive disease model, which provides a new murine model of WNV-induced spatial memory impairment, and identifies a potential mechanism underlying neurocognitive impairment in patients recovering from WNV Neuroinvasive Disease.
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Altered Axonal Mitochondrial Transport in the Pathogenesis of Charcot-Marie-Tooth Disease from Mitofusin 2 Mutations
TL;DR: In this article, the authors explore the mechanism by which mutations in the mitochondrial fusion protein mitofusin 2 (MFN2) lead to neuropathy and explore how MFN2 mutations lead to degeneration of peripheral axons.