J
Jeffrey D. Rothstein
Researcher at Johns Hopkins University School of Medicine
Publications - 350
Citations - 59672
Jeffrey D. Rothstein is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Glutamate receptor. The author has an hindex of 111, co-authored 332 publications receiving 53109 citations. Previous affiliations of Jeffrey D. Rothstein include University of Sheffield & Johns Hopkins University.
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Journal ArticleDOI
A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD
Alan E. Renton,Elisa Majounie,Adrian James Waite,Javier Simón-Sánchez,Javier Simón-Sánchez,Sara Rollinson,J. Raphael Gibbs,J. Raphael Gibbs,Jennifer C. Schymick,Hannu Laaksovirta,John C. van Swieten,John C. van Swieten,Liisa Myllykangas,Hannu Kalimo,Anders Paetau,Yevgeniya Abramzon,Anne M. Remes,Alice Kaganovich,Sonja W. Scholz,Sonja W. Scholz,Sonja W. Scholz,Jamie Duckworth,Jinhui Ding,Daniel W. Harmer,Dena G. Hernandez,Dena G. Hernandez,Janel O. Johnson,Janel O. Johnson,Kin Y. Mok,Mina Ryten,Danyah Trabzuni,Rita Guerreiro,Richard W. Orrell,James Neal,Alexandra Murray,J. P. Pearson,Iris E. Jansen,David Sondervan,Harro Seelaar,Derek J. Blake,Kate Young,Nicola Halliwell,Janis Bennion Callister,Greg Toulson,Anna Richardson,Alexander Gerhard,Julie S. Snowden,David M. A. Mann,David Neary,Mike A. Nalls,Terhi Peuralinna,Lilja Jansson,Veli-Matti Isoviita,Anna-Lotta Kaivorinne,Maarit Hölttä-Vuori,Elina Ikonen,Raimo Sulkava,Michael Benatar,Joanne Wuu,Adriano Chiò,Gabriella Restagno,Giuseppe Borghero,Mario Sabatelli,David Heckerman,Ekaterina Rogaeva,Lorne Zinman,Jeffrey D. Rothstein,Michael Sendtner,Carsten Drepper,Evan E. Eichler,Can Alkan,Ziedulla Abdullaev,Svetlana Pack,Amalia Dutra,Evgenia Pak,John Hardy,Andrew B. Singleton,Nigel Williams,Peter Heutink,Stuart Pickering-Brown,Huw R. Morris,Huw R. Morris,Huw R. Morris,Pentti J. Tienari,Bryan J. Traynor,Bryan J. Traynor +85 more
TL;DR: The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases, and a large hexanucleotide repeat expansion in the first intron of C9ORF72 is shown.
Journal ArticleDOI
Knockout of Glutamate Transporters Reveals a Major Role for Astroglial Transport in Excitotoxicity and Clearance of Glutamate
Jeffrey D. Rothstein,Margaret Dykes-Hoberg,Carlos A. Pardo,Lynn A. Bristol,Lin Jin,Ralph W. Kuncl,Yoshikatsu Kanai,Matthias A. Hediger,Yanfeng Wang,Jerry P Schielke,Devin Franklin Welty +10 more
TL;DR: It is suggested that glial glutamate transporters provide the majority of functional glutamate transport and are essential for maintaining low extracellular glutamate and for preventing chronic glutamate neurotoxicity.
Journal ArticleDOI
Identification of a unique TGF-β–dependent molecular and functional signature in microglia
Oleg Butovsky,Mark P. Jedrychowski,Craig S. Moore,Ron Cialic,Amanda J. Lanser,Galina Gabriely,Thomas Koeglsperger,Ben Dake,Pauline M. Wu,Camille Doykan,Zain Fanek,LiPing Liu,Zhuoxun Chen,Jeffrey D. Rothstein,Richard M. Ransohoff,Steven P. Gygi,Jack P. Antel,Howard L. Weiner +17 more
TL;DR: It is found that TGF-β was required for the in vitro development of microglia that express the microglial molecular signature characteristic of adultmicroglia and that microglian were absent in the CNS of TGF -β1–deficient mice.
Journal ArticleDOI
Localization of neuronal and glial glutamate transporters
Jeffrey D. Rothstein,Lee J. Martin,Allan I. Levey,Margaret Dykes-Hoberg,Lin Jin,David Wu,Norman Nash,Ralph W. Kuncl +7 more
TL;DR: The cellular and subcellular distributions of the glutamate transporter subtypes EAAC1, GLT-1, and GLAST in the rat CNS were demonstrated using anti-peptide antibodies that recognize the C-terminal domains of each transporter.
Journal ArticleDOI
Selective loss of glial glutamate transporter GLT-1 in amyotrophic lateral sclerosis.
TL;DR: Developing C‐terminal, antioligopeptide antibodies that were specific for each glutamate transporter subtype found that GLT‐1 immunoreactive protein was severely decreased in ALS, both in motor cortex (71% decrease compared with control) and in spinal cord.