Mady Hornig, MD, MA, is Associate Professor of Epidemiology and Director of Translational Research in the Jerome L. and Dawn Greene Infectious Disease Laboratory at the Mailman School of Public Health, Columbia University. A physician-scientist, she is widely recognized for her animal model and clinical research on the role of microbial, immune, and toxicologic factors in neuropsychiatric disorders, including autism, schizophrenia, attention-deficit/hyperactivity disorder, obsessive-compulsive disorder, and mood disorders. Her work integrates data from animal models and epidemiologic studies to understand the mechanisms by which environmental factors, including viruses, bacteria, and toxins, or common host responses to these agents during brain maturation, may act as triggers or amplifying factors in the pathogenesis of some neuropsychiatric conditions. Findings from animal models of immune-mediated neurodevelopmental damage are employed to sharpen the focus of investigations in human cohorts, creating the basis for translation into novel biomarkers and intervention strategies; and hypotheses generated from epidemiologic studies are rigorously tested in animal models. In 2004, Dr. Hornig presented to the Institute of Medicine Immunization Safety Review Committee and testified twice before congressional subcommittees regarding the role of infections and toxins in autism pathogenesis. She leads a project on immune and neuroendocrine factors in West Nile virus encephalitis within the Northeast Biodefense Center, an NIAID regional center of excellence in biodefense and emerging infectious diseases, where she is a member of the Core Oversight Committee and the Governing Council. She was recently elected to the President's Council of Cornell Women.
Honors & Awards
Areas of Expertise
Select Global Activities
Gene-Environment Interactions in an Autism Birth Cohort, Norway: This project will describe the developmental trajectory of children with autism spectrum disorders, identify risk factors associated with the development of these disorders, and elucidate biologic markers (genetic, biochemical) present before or at birth that may help to predict children at risk for the development of these disorders.
Hornig M, Mozley PD, Amsterdam JD HMPAO SPECT brain imaging in treatment-resistant depression Prog Neuro-Psychopharmacol Biol Psychiatry 21 1097-114 1997
Hornig M, Goodman DBP, Kamoun M, Amsterdam JD Positive and negative acute phase proteins in affective subtypes J Affective Disord 49 9-18 1998
Hornig M, Amsterdam JD, Kamoun M, Goodman DBP Autoantibody disturbances in affective disorders: a function of age and gender? J Affective Disord 55 29-37 1999
Hornig M, WeissenbÃ¶ck H, Horscroft N, Lipkin WI An infection-based model of neurodevelopmental damage Proc Natl Acad Sci USA 96 12102-7 1999
Weissenbock H, Hornig M, Hickey WF, Lipkin WI Microglial activation and neuronal apoptosis in Bornavirus infected neonatal Lewis rats Brain Pathol 10 260-72 2000
Hornig-Rohan M, Amsterdam JD Venlafaxine versus stimulant therapy in patients with dual diagnosis ADD and depression Prog Neuro-Psychopharmacol Biol Psychiatry 26 585-9 2002
Hoffman KL, Hornig M, Yaddanapudi K, Jabado O, Lipkin WI A murine model for neuropsychiatric disorders associated with group A beta-hemolytic streptococcal infection J Neurosci 24 1780-91 2004
Hornig M, Chian D, Lipkin WI Neurotoxic effects of postnatal thimerosal are mouse strain-dependent (advance online publication) Molec Psychiatry 8 June 2004 doi:10.1038/sj/mp.4001529 2004
Hornig M, Lipkin WI Infectious and immune factors in the pathogenesis of neurodevelopmental disorders: epidemiology, hypotheses, and animal models Mental Retardation Dev Disabil Res Rev 7 200-10 2001
Lipkin WI, Hornig M Neurovirology. Microbes and the brain. Lancet 352 SIV21 1999