Chair, Department of Neurology
Director, Neuroscience Research Institute
Co-director, Neurological Institute
Stanley D. and Joan H. Ross Chair of Neuromodulation
Clinical interests:Multiple Sclerosis (MS)
Research Interests: Multiple Sclerosis (MS) and Neuroimmunology
Current Research: New neutrophil subset promotes CNS neuron survival and axon regeneration
Education:
Brown University, 1988
Postgraduate:
Residency: Memorial Sloan Kettering Cancer Center, Neurology, NY, 1992
Board Certification: Neurology
As of July 1, 2019 Benjamin M. Segal, MD, assumed the roles of chair of the Department of Neurology and Director of the Neurological Research Institute at The Ohio State University College of Medicine. He is also co-director of The Ohio State University Wexner Medical Center’s Neurological Institute. He earned his medical degree Brown University, completed his internship in medicine at University of Chicago and conducted his residency in neurology at New York Hospital/Weill Medical College of Cornell University.
Dr. Segal began his academic career at the National Institutes of Health (NIH), where he conducted innovative research in multiple sclerosis and immunology. In 2000, he was recruited to the Department of Neurology at the University of Rochester. That year he was awarded the prestigious Harry Weaver Neuroscience Scholar award by the National Multiple Sclerosis Society. The University of Michigan—home to one of our nation’s top neurology programs—recruited Dr. Segal to lead its Division of Multiple Sclerosis in 2007. Under Dr. Segal’s leadership, the University of Michigan became a national referral center for the treatment of patients with multiple sclerosis. The MS clinic population expanded in size from approximately 400 to 4,000 patients during his tenure.
Dr. Segal is internationally recognized for his work in multiple sclerosis (MS) and neuroimmunology. With annual NIH funding for his ongoing research programs in excess of 1.3 million dollars, his discoveries have contributed to the basic understanding of the pathogenesis of multiple sclerosis (MS) and similar diseases. He has shown that the type of inflammation that causes damage to the nervous system during MS can vary among individuals, suggesting that pharmaceutical regimens must be personalized for each patient. Dr. Segal has directed a number of industry- and government-sponsored clinical trials and biomarker studies that focus on individuals with relapsing and progressive forms of the disease. More recently, his laboratory is investigating how destructive immune responses in the nervous system can be skewed and redirected to initiate repair. He publishes in high impact academic journals, including the Journal of Clinical Investigation,Annals of Neurology, Proceedings of the National Academy of Sciences of the United States of America, and Lancet Neurology.
Dr. Segal has received innumerable awards, lectured nationally and internationally and served on multiple NIH study sections, including co-chairing the major review panel in his field. He holds several patents and is a member of every major organization in neurology. Dr. Segal served as Program Chair for the annual meeting of the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS) between 2016 and 2018, and he currently serves as a Director at ACTRIMS. Through ACTRIMS, he has developed an annual national symposium to educate neurology residents and young research investigators about the diagnosis, pathogenesis, and treatment of MS. Dr. Segal was inducted into the University of Michigan League of Research Excellence in 2014. He was a Senior Scholar of the A. Alfred Taubman Medical Research Institute and has been named among the Best Doctors in America for the past eight years.
Segal BM. Modulation of the Innate Immune System: A Future Approach to the Treatment of Neurological Disease. Clin. Immunol. 2018;189:1-3. PMID: 29628125
Segal BM, Cohen JA, Antel J. Americas Committee for Treatment and Research in Multiple Sclerosis Forum 2017: Environmental factors, genetics and epigenetics in MS susceptibility and clinical course. Mult Scler 2018;24(1): 4-5. PMID: 29307302
Giles, DA, Washnock-Schmid JM, Duncker PC, Dahlawi S, Ponath G, Pitt D, Segal BM. Myeloid cell plasticity in the evolution of central nervous system autoimmunity. Ann Neuro 2018;83(1): 131-141. PMID: 29283442
Duncker PC, Stoolman JS, Huber AK, Segal BM. GM-CSF Promotes Chronic Disability in Experimental Autoimmune Encephalomyelitis by Altering the Composition of Central Nervous System-Infiltrating Cells, but is Dispensable for Disease Induction. J Immunol 2018; 200(3): 966-973. PMID: 29288202
Neal LM, Xing E, Xu J, Kolbe J, Osterholzer JJ, Segal BM, Williamson PR, Olszewski, MA. CD4+ T cells orchestrate lethal immune pathology despite fungal clearance during Cryptococcus neoformans meningoencephalitis. mBio. 2017;8(6): pii: e01415-17. PMID: 29162707
Klein RS, Voskuhl R, Segal BM, Dittel BN, Lane TE, et. al. Speaking out about gender imbalance in invited speakers improves diversity. Nat. Immunol. 2017;18(5): 475-478. PMID: 28418385
Dickerson EC, Davenport MS, Syed FI, Stuve O, Cohen JA, Rinker J, Goldman MD, Segal BM, Foerster BR. Effect of template reporting of brain MRIs for multiple sclerosis on report thoroughness and neurologist rated quality: results of a prospective quality improvement project. J Am Coll Radiol. 2017;14(3): 371-379.e1. PMID: 27932248
Cravens PD, Hussain RZ, Miller-Little WA, Ben L, Segal BM, Herndon E, Stuve O. IL-12/IL-23p40 Is Highly Expressed in Secondary Lymphoid Organs and the CNS during All Stages of EAE, but Its Deletion Does Not Affect Disease Perpetuation. PLOS ONE 2016; 11(10): e0165248. PMID: 27780253
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;13(1): 178. PMID: 27391474
Huber AK, Giles DA, Segal BM, Irani DN. An emerging role of eotaxins in neurodegenerative disease. Clin Immunol. 2016; Epub. PMID: 27664933
Segal BM and Giger RJ. Stable biomarker for plastic microglia. Proc Nat Acad Sci USA 2016; 113(12):3130-2. PMID: 26966229
Segal BM and Stuve O. Clinical trials in primary progressive multiple sclerosis- why we are failing. The Lancet. 2016;387(10023): 1032-4. PMID: 26827076
Phares TW, DiSano KD, Stohlman SA, Segal BM, Bergmann CC. CXCL13 promotes isotype switched B cell accumulation to the central nervous system during viral encephalomyelitis. Brain Behav Immun 2016;54: 128-39. PMID: 26795429
Grifka-Walk HM and Segal BM. T-bet promotes the accumulation of encephalitogenic Th17 cells in the CNS. J. Neuroimmunol 2016;304: 35-39. PMID: 27242075
Grifka-Walk HM, Giles DA, Segal BM. IL-12 polarized Th1 cells produce GM-CSF and induce EAE independent of IL-23. Eur J Immunol 2015;45(10): 2780-6, PMID: 26220255
Carbajal K, Mironova Y, Ulrich-Lewis J, Kalkarni D, Grifka-Walk H, Huber A, Shrager P, Segal BM. Th Cell Diversity in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis. J Immunol 2015; 195(6):2552-9. PMID: 26238492
Murdock BJ, Bender DE, Segal BM, Feldman EL. The dual roles of immunity in ALS: Injury overrides protection. Neurobiol Dis 2015;77: 1-12. PMID: 25726748
Baldwin KT, Carbajal KS, Giger RJ*, Segal BM*. Neuroinflammation triggered by a beta-glucan/dectin-1 signaling enables CNS regeneration. Proc Nat Acad Sci USA 2015;112(8): 2581-6. PMID: 25675510
Rumble JM, Huber AK, Krishnamoorthy G, Srinivasan A, Giles DA, Zhang X, Wang L, Segal BM. Neutrophil-related factors as biomarkers in EAE and MS. J Exp Med 2015;212(1): 23-35. PMID: 25559893
