Jeffrey L. Elliott, M.D., is a Professor in the Department of Neurology at UT Southwestern Medical Center. He specializes in neuromuscular disorders.
Dr. Elliott earned his medical degree at Washington University School of Medicine in St. Louis. He completed a residency in neurology at Barnes-Jewish Hospital and received advanced training through a neuromuscular disease fellowship at Washington University Medical Center.
Certified by the American Board of Psychiatry and Neurology and the American Board of Electrodiagnostic Medicine, he joined the UT Southwestern faculty in 1997.
Dr. Elliott is head of the neuromuscular section of the neuromuscular division in the Department of Neurology and is Director of the MDA/ALS Clinic at UT Southwestern. He’s a member of the American Academy of Neurology, the American Neurological Association, and the American Association of Neuromuscular & Electrodiagnostic Medicine. In 2018, he earned the Trephined Cranium Award for Excellence in Neurology Teaching.
- Medical School
- Washington University School of Medicine (1988)
- Jewish Hospital of St. Louis (1989), Internal Medicine
- Barnes-Jewish Hospital (1992), Neurology
- Washington University in St. Louis (1994), Neuromuscular Disease
- Amyotrophic Lateral Sclerosis; Energetics
- MicroRNA-206 delays ALS progression and promotes regeneration of neuromuscular synapses in mice.
- Williams AH, Valdez G, Moresi V, Qi X, McAnally J, Elliott JL, Bassel-Duby R, Sanes JR, Olson EN Science 2009 Dec 326 5959 1549-54
- Redox susceptibility of SOD1 mutants is associated with the differential response to CCS over-expression in vivo.
- Son M, Fu Q, Puttaparthi K, Matthews CM, Elliott JL Neurobiol. Dis. 2009 Apr 34 1 155-62
- The death domain-containing kinase RIP1 regulates p27(Kip1) levels through the PI3K-Akt-forkhead pathway.
- Park S, Ramnarain DB, Hatanpaa KJ, Mickey BE, Saha D, Paulmurugan R, Madden CJ, Wright PS, Bhai S, Ali MA, Puttaparthi K, Hu W, Elliott JL, Stuve O, Habib AA EMBO Rep. 2008 Aug 9 8 766-73
- Biological effects of CCS in the absence of SOD1 enzyme activation: implications for disease in a mouse model for ALS.
- Proescher JB, Son M, Elliott JL, Culotta VC Hum. Mol. Genet. 2008 Jun 17 12 1728-37
- Isolated cytochrome c oxidase deficiency in G93A SOD1 mice overexpressing CCS protein.
- Son M, Leary SC, Romain N, Pierrel F, Winge DR, Haller RG, Elliott JL J. Biol. Chem. 2008 May 283 18 12267-75
- Assessing the role of immuno-proteasomes in a mouse model of familial ALS.
- Puttaparthi K, Van Kaer L, Elliott JL Exp. Neurol. 2007 Jul 206 1 53-8
- Overexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitochondrial pathology.
- Son M, Puttaparthi K, Kawamata H, Rajendran B, Boyer PJ, Manfredi G, Elliott JL Proc. Natl. Acad. Sci. U.S.A. 2007 Apr 104 14 6072-7
- Novel mutations that enhance or repress the aggregation potential of SOD1.
- Krishnan U, Son M, Rajendran B, Elliott JL Mol. Cell. Biochem. 2006 Jul 287 1-2 201-11
- Non-neuronal induction of immunoproteasome subunits in an ALS model: possible mediation by cytokines.
- Puttaparthi K, Elliott JL Exp. Neurol. 2005 Dec 196 2 441-51
- Beginning to understand hereditary spastic paraplegia atlastin.
- Elliott JL Arch. Neurol. 2004 Dec 61 12 1842-3
A 63 year old man with nausea, vomiting and orthostatic dizziness and distal limb paresthesia. In A case based guide to Neuromuscular Pathology
Elliott JL, Zhou L, Cai C, Kaku M (2019). Springer
Honors & Awards
- Trephined Cranium Award for Excellence in Neurology Teaching
Awarded for recognition for excellence in Neurology teaching by neurology residents (2018-2019)
- President Research Council Distinguished Young Researcher Award
- American Neurological Association (2005-2020)
- American Academy of Neurology
- American Association of Electrodiagnostic Medicine