Abdolmohamad Rostami, MD, PhD
Professor and Chair, Department of Neurology
Vickie and Jack Farber Institute for Neuroscience

Contact
900 Walnut Street
Suite 200
Philadelphia, PA 19107
215-955-1234
215-955-1390 fax
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Abdolmohamad Rostami, MD, PhD
Professor and Chair, Department of Neurology
Vickie and Jack Farber Institute for Neuroscience
Research & Clinical Interests
My research focuses on...
Multiple Sclerosis is an autoimmune disease of the central nervous system that affects over 400,000 Americans and over 2 million worldwide. My research focuses on the pathogenesis of multiple sclerosis using the animal model of this disease, experimental autoimmune encephalomyelitis (EAE). At the present, we are focusing on three main areas:
1) The role of IL-12/IL-17/IL-23 axis in the pathogenesis of EAE and multiple sclerosis.
Specifically, studies will examine IL-12/IL-17/IL-23 produced by antigen presenting cells (APC) from the periphery (macrophages and dendritic cells) and from the central nervous system (CNS) microglia in EAE. In addition to a better understanding of the pathogenesis of inflammatory demyelination, the information derived from this study will be helpful if these cytokines are to be considered as targets for therapy in MS.
2) The effect of the Bowman-Birk protease inhibitor on the course of EAE. This study has the potential to provide a novel, safe, and effective therapy for multiple sclerosis.
3) Mechanisms of intravenous tolerance in EAE.
This study will elucidate the mechanisms by which intravenous myelin antigens induce tolerance and suppress clinical disease in EAE. This study will provide a novel method for analyzing the migration and functional status of infiltrating cells in the CNS, in particular, and in target organs of other autoimmune diseases. It has the potential as a possible therapy for autoimmune diseases."
Education
Medical School: Shiraz University
Residency: Hospital of University of Pennsylvania (HUP)
Fellowship: Hospital of University of Pennsylvania (HUP)
Publications
- Retraction Notice to: Neural Stem Cells Engineered to Express Three Therapeutic Factors Mediate Recovery from Chronic Stage CNS Autoimmunity (Molecular Therapy (2016) 24(8) (1456–1469), (S1525001616335973), (10.1038/mt.2016.104))
- Corrigendum: Combination therapy with fingolimod and neural stem cells promotes functional myelination in vivo through a non-immunomodulatory mechanism(Front. Cell. Neurosci., (2019), 13, (14), 10.3389/fncel.2019.00014)
- GATA1 controls numbers of hematopoietic progenitors and their response to autoimmune neuroinflammation
- SIRT1 inactivation switches reactive astrocytes to an antiinflammatory phenotype in CNS autoimmunity
- Transcription Factor RUNX3 Mediates Plasticity of ThGM Cells Toward Th1 Phenotype
Board Certification
Neurology
Hospital Appointment
Thomas Jefferson University Hospital
Methodist Hospital Division of Thomas Jefferson University Hospital