Michael C. Levin, M.D.

Michael C. Levin, M.D.

Associate Professor
Department of Neurology
Department of Anatomy and Neurobiology

The University of Tennessee Health Science Center
855 Monroe Avenue, Room 415
Memphis, TN 38163
Phone: (901) 448-2243
Fax: (901) 448-7440
Email: Michael C. Levin


  • M.D. Institution: The Milton S. Hershey Medical Center, Pennsylvania State University
  • Postdoctoral: National Institutes of Health, Neuroimmunology Branch


Research Interests

This laboratory studies the relationship between viruses and immune-associated diseases of the human central nervous system, particularly multiple sclerosis (MS). Specifically, they study how patients infected with HTLV-1 (human T - lymphotropic virus type I) develop HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP), a demyelinating disease with similarities to MS. Current experiments focus on two major areas. First, identifying a novel auto-antibody response in HAM/TSP patients that may identify a human protein with similarities to viral proteins, an area of study known as molecular mimicry. Second, experiments are designed to identify abnormal expression of RNA using single cell analysis of abnormal areas of brain from MS and HAM/TSP patients. By identifying what cells produce in the central nervous system they hope to develop novel therapeutic strategies to help treat patients with these diseases.

Representative Publications

  • Levin MC, Lee S, Gardner LA, Shin Y, Douglas JN, Salapa H. Autoantibodies to heterogeneous nuclear ribonuclear protein A1 (hnRNPA1) cause altered 'ribostasis' and neurodegeneration; the legacy of HAM/TSP as a model of progressive multiple sclerosis. J Neuroimmunol. 2017 Mar 15;304:56-62. doi: 10.1016/j.jneuroim.2016.07.005. Epub 2016 Jul 17. PubMed PMID: 27449854.
  • Douglas JN, Gardner LA, Salapa HE, Lalor SJ, Lee S, Segal BM, Sawchenko PE, Levin MC. Antibodies to the RNA-binding protein hnRNP A1 contribute to neurodegeneration in a model of central nervous system autoimmune inflammatory disease. J Neuroinflammation. 2016 Jul 8;13(1):178. doi: 10.1186/s12974-016-0647-y. PubMed PMID: 27391474; PubMed Central PMCID: PMC4938923.
  • Drevinge C, Dalen KT, Mannila MN, Täng MS, Ståhlman M, Klevstig M, Lundqvist A, Mardani I, Haugen F, Fogelstrand P, Adiels M, Asin-Cayuela J, Ekestam C, Gådin JR, Lee YK, Nebb H, Svedlund S, Johansson BR, Hultén LM, Romeo S, Redfors B, Omerovic E, Levin M, Gan LM, Eriksson P, Andersson L, Ehrenborg E, Kimmel AR, Borén J, Levin MC. Perilipin 5 is protective in the ischemic heart. Int J Cardiol. 2016 Sep 15;219:446-54. doi: 10.1016/j.ijcard.2016.06.037. Epub 2016 Jun 16. PubMed PMID: 27376234.
  • Douglas JN, Gardner LA, Salapa HE, Levin MC. Antibodies to the RNA Binding Protein Heterogeneous Nuclear Ribonucleoprotein A1 Colocalize to Stress Granules Resulting in Altered RNA and Protein Levels in a Model of Neurodegeneration in Multiple Sclerosis. J Clin Cell Immunol. 2016 Apr;7(2):402. Epub 2016 Mar 22. PubMed PMID: 27375925; PubMed Central PMCID: PMC4928374.
  • Klevstig M, Ståhlman M, Lundqvist A, Scharin Täng M, Fogelstrand P, Adiels M, Andersson L, Kolesnick R, Jeppsson A, Borén J, Levin MC. Targeting acid sphingomyelinase reduces cardiac ceramide accumulation in the post-ischemic heart. J Mol Cell Cardiol. 2016 Apr;93:69-72. doi: 10.1016/j.yjmcc.2016.02.019. Epub 2016 Feb 28. PubMed PMID: 26930027; PubMed Central PMCID: PMC5026316.
  • Gardner LA, Levin MC. Importance of Apolipoprotein A-I in Multiple Sclerosis. Front Pharmacol. 2015 Nov 20;6:278. doi: 10.3389/fphar.2015.00278. eCollection 2015. Review. PubMed PMID: 26635608; PubMed Central PMCID: PMC4654019.

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