Staley A. Brod, M.D.

Professor of Neurology

Contact Information:

• Phone: 713-500-7135
  
• Fax: 713-500-7040
  
• E-mail: Staley.A.Brod@uth.tmc.edu

Board Certifications

• American Board of Psychiatry and Neurology in Neurology
• American Board of Internal Medicine in Internal Medicine

Education and Training:

• Undergraduate: Western Reserve Academy, A.B. Williams College - Major in Philosophy/Chemistry
• Medical School: University of Toledo, Ohio
• Internal Medicine Residency: Medical College of Ohio
• Neurology Residency: Yale-New Haven Medical Center, Yale University Medical School
• Research and Clinical Neurology Fellowship: Center for Neurologic Disease, Brigham and Women’s Hospital, Harvard Medical School, Boston

Clinical & Research Interests

The goal of my proposed research is to investigate whether oral ACTH has an immunological effect at low doses without absorption and immunological/endocrinological effects with absorption at higher doses in subjects with MS. If we can define optimal dose(s) producing immunological effect (non-absorption – activity mediated by non-adrenal melanocortin receptors) and endocrinological (non-absorption & absorption – mediated by adrenal MC2 exclusively), we can design trails to compare 1) oral ACTH to standard IV steroids using clinical recovery after relapse as primary outcome & reduced MRI activity as secondary outcome measures in phase II RCT and 2) oral ACTH ± DMT using time to 1st relapse as primary outcome measure and reduction ARR and MR activity as secondary outcome measure.

My pilot clinical trial with small numbers of normal volunteers showed that oral ACTH at the upper limit of typical parenteral doses altered PMNC IL-1 and IL-17 secretion. There was a trend suggesting absorption at the highest dose tested (120 IU). Therefore, we will determine whether oral ACTH decreases ex vivo IL-17 secretion in a dose dependent way in MS patients and which lymphocyte population is responsible for IL-17 immunomodulation.

An alternative form of ACTH (oral) without such side effects would be useful if absorption is achieved. Oral ACTH may beneficially interact with the gut associated immune system (GALT), generating immunomodulation, and as an endogenous peptide found in humans, may have a high therapeutic index. At higher doses, oral ACTH may be absorbed and elevate serum ACTH levels resulting in increased serum cortisol.

Combination therapy of an acute anti-inflammatory agent such as ACTH to traditional disease modifying therapies may provide additive beneficial effects on brain inflammation (MR), relapses and progression without switching to immunosuppressive agents.

Biography

Staley A. Brod, M.D., has been a Professor of Neurology at the University of Texas Health Science Center, Houston School of Medicine, since 2002. He attended medical school at the Medical College of Ohio, graduating in 1981. He went on to complete a residence in neurology at the Yale-New Haven Medical Center, Yale University Medical School. Following his residency, Dr. Brod was a Distinguished Research and Clinical Fellow in Neurology from 1987-1990 (National Multiple Sclerosis Society award) at the Center for Neurologic Disease, Brigham and Women's Hospital, Harvard Medical School. Dr. Brod is Board certified in Internal Medicine and Neurology.

Dr. Brod has received funding from the National Multiple Sclerosis Society, as well as the pharmaceutical industry for his involvement in conducting clinical trials of investigational drugs for the treatment of multiple sclerosis, including interferons, anti-inflammatory agents, and monoclonal antibodies. Dr. Brod has been the principal investigator for four phase II & IV clinical trials in multiple sclerosis and is following the progress of over 700 patients with multiple sclerosis. His current research interests include animal models of auto-immune disease; immunomodulation; counter regulatory cytokines; multiple sclerosis (MS), oral ACTH and somatostatin for the treatment of MS, and novel therapeutics for the treatment of MS.

Dr. Brod is a member of the American Academy of Neurology and the International Society for Interferon and Cytokine Research and the International Cytokine Society, and is a member of the Clinical Advisory Committee for the Lone Star Chapter of the National Multiple Sclerosis Society. Dr. Brod has received numerous distinguished awards, including the National Research Service Award from the National Institutes of Health and the National Multiple Sclerosis Society Barbara Jordan Research Award. Dr. Brod has been named America’s Top Physicians by the Consumers’ Research Council of America in 2004, 2010 and 2011 and was honored with the 2011 Patient’s Choice Award from Consumer Research. Dr. Brod is a 2011 Top Doctor in Who’s Who and Who’s Who Professional of the Year 2010. Dr. Brod has published over 130 abstracts and papers on autoimmunity in animal models and humans. He also serves as a reviewer for many medical journals including Journal of Immunology, Journal of Neuroimmunology, Annals of Neurology, Archives of Neurology, and Neurology.

Recent Publications

• KI Rother, RJ Brown, M. Morales, E. Wright, Z. Duan, C Campbell, DM Harlan, PR Orlander, SA Brod. Ingested IFN-Alpha2a Prolongs the ‘Honeymoon’ Phase in New Onset Type 1 Diabetes Mellitus (T1D) in a phase II Randomized clinical trial (RCT). 10th IDS Congress. Malmo, Sweden, May 2009.
• Brod SA, Z Hood. 2008. Evaluation of Plasma Cortisol Concentrations after Subcutaneous and Intramuscular Administration of H.P. Acthar® Gel in Healthy Volunteers. Biomed & Pharmacother Sept 17, pg 1-3.
• K Rother, D. Harlan, Dana Hardin, Philip Orlander, Patrick Brosnan, Victor Lavis, S. Brod. Ingested Interferon Alpha: Prolongation or Permanence of the ‘Honeymoon’ Phase in Newly Diagnosed Diabetes Mellitus. Diabetes Care 32(7): 1250-5.
• Brod SA, Khan M, Nelson LD, Decuir B, Malone M, and Henninger E. Adoptive Transfer of Activated T and CD8+ T cells from Murine IFN-??Fed Donor Mice Inhibits Actively Induced Experimental Autoimmune Encephalomyelitis in Recipients and is Associated with Decreasing TNF-? Secretion. J. Immunother. 2000; 23(2): 235-245.
• Brod S, JW Lindsey, and JS Wolinsky. Combination Therapy with Glatirimer Acetate (Copolymer-1) and a Type I Interferon (IFN-?) Does Not Improve Experimental Autoimmune Encephalomyelitis. Ann Neurol 2000;47: 127-131.
• Brod S, Phan T, Katz S, and Stepkowski S. Ingested IFN-b delays islet allograft rejection. Transplantation. 2000; 69 (10), 2162-6.
• Brod SA. 2000. Unregulated Inflammation Shortens Human Functional Longevity. Inflammation Res 49:561-70.
• Brod SA. Friedman AW, Appleyard J, Warner NB. 2000. Ingested IFN-b has biological effects in rheumatoid arthritis. Int. J Immunother 16 (3-4), 53.
• Brod SA, Lindsey JW, Vriesendorp FS, Ahn C, Narayana PA, Wolinsky JS. 2001. Ingested IFN-a: Results of a pilot study in relapsing-remitting multiple sclerosis (RRMS). Neurology 57 (5): 845-852.
• Brod S, Orlander P, Lavis V, Brosnan P, Hardin D, Henninger E, and Riley W. 2001. Ingested IFN-a ?prolongs the “honeymoon” period in newly diagnosed type I diabetes mellitus. J Interferon Cyt Res 21 (11), 1021-1030.
• Brod SA. 2002. Ingested Type I Interferon – State of the art in the Treatment of Autoimmunity. Experimental Biology and Medicine 227(11): 981-8.
• Brod SA. 2002. Ingested Type I Interferon – A Potential Treatment for Autoimmunity. J Interferon Cyt Res 22 (12) pp 1153-1166.
• Brod SA, M Nguyen, Z Hood, G Shipley. 2006. Ingested (oral) IFN-alpha represses TNF-alpha mRNA in relapsing-remitting multiple sclerosis. J Interferon Cyt. Res. Mar;26(3):150-5.
• Brod SA, Z Hood. 2007. Ingested (oral) SIRS Peptide 1-21 Inhibits Acute EAE By Inducing Th2-like Cytokines. J Neuroimmunol Feb 183 (1-2): 89-95.
• Brod SA, Z Hood. 2008. Ingested (oral) SIRS Peptide 1-21 Suppresses T1DM in NOD mice. J Interferon Cyt Res 28 (1): 25-30.
• Brod SA, Z Hood. Ingested (oral) alpha-MSH Inhibits Acute EAE. 2008. J Neuroimmunol. 193: 106-112.
• Brod SA, Z Hood. Evaluation of Plasma Cortisol Concentrations after Subcutaneous and Intramuscular Administration of H.P. Acthar® Gel in Healthy Volunteers. Biomed & Pharmacother Sept 17, pg 1-3.
• K Rother, D. Harlan, Dana Hardin, Philip Orlander, Patrick Brosnan, Victor Lavis, S. Brod. Ingested Interferon Alpha: Prolongation or Permanence of the ‘Honeymoon’ Phase in Newly Diagnosed Diabetes Mellitus. Diabetes Care 32(7): 1250-5.
• Brod SA. 2010 Ingested Type I Interferon – State of the Art as Treatment for Autoimmunity Part 2, Pharmaceuticals3(4): 1108-1121.
• Brod SA, Z Hood. 2011. Ingested (oral) ACTH (Adreno-Cortico-Tropic Hormone) Inhibits EAE J Neuroimmunol., 232, 131-5.
• Brod SA, Z Hood. 2011. Ingested (oral) SST (somatostatin) Inhibits EAE. Autoimmunity 44 (5), 437-43

Patents

• D-5716 CIP5
  USPTO USSN 09/314,503
  “Method of Treating Auto-Immune Diseases Using Type One Interferons”
  Inhibition of Transplant Rejection by Type I Interferon.
  Patent Number 6,346,243
• D-5716 EPC
  European Patent Application No. 95916293.4
  “Method of Treating Auto-Immune Diseases Using Type One Interferons”
  Patent Number 0752884
• D-5716
  Japanese Patent Application No. 07-526,504
  “Method of Treating Auto-Immune Diseases Using Type One Interferons”
• D-6380—USPTO
  USSN 007625554B2
  Date of Patent December 1, 2009
  “Treatment of Cognitive Decline”
• US Patent 7,807,143
  “Alpha-MSH Therapies for the Treatment of Autoimmune Diseases”
• CLFR:253WO
  “Immune Response Suppressor and Treatment of Multiple Sclerosis”
• D-5716CIP4/C—USPTO
  “Method of Treating Auto-Immune Diseases Using Type One Interferons”
  Rheumatoid Arthritis
  Notice of Allowance April 12, 2010.