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Mady Hornig

Mady Hornig, MD, is a psychiatrist and an associate professor of epidemiology at Columbia University's Mailman School of Public Health, where she is Director of Translational Research in the Center for Infection and Immunity (CII). A physician-scientist, her research involves clinical, epidemiologic, and animal model research on autism and related neurodevelopmental conditions. She directs the clinical core of an international investigation of the role of Borna disease virus in human mental illness and participates as a key investigator for the Autism Birth Cohort (ABC) project, a large prospective epidemiologic study based in Norway that is identifying how genes and timing interact with environmental agents to lead to autism and other neurodevelopmental conditions. In 2006, she was appointed as Guest Professor at the School of Basic Medical Science of Beijing University in Beijing, China.

Hornig is investigating the role of viral and immune factors affecting mental health. Along with CII director, W. Ian Lipkin, and colleague, Thomas Briese, she is currently investigating measles virus DNA sequences in bowel biopsies of children with autism spectrum disorders. Formulating a ‘three strikes’ model of causation that integrates genetics, the environment and developmental neurobiology, Hornig posits that some cases of autism may represent the unfortunate coincidence of genetic vulnerability (first dimension) and exposure to environmental factors (second dimension) at a critical period of brain development (third dimension). She is examining how brain damage from infections, immune system dysfunction, neurotoxins, and other chemical or psychosocial stressors, or host responses to these environmental agents, can lead to neurodevelopmental and other central nervous system disorders, thereby contributing to autism, schizophrenia, attention deficit hyperactivity disorder, obsessive compulsive disorders, and mood disorders.

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Dr. Hornig received a bachelor's degree in 1978 from Cornell University, where she was a College Scholar; an MA in psychology in 1983 from the New School for Social Research, and an MD in 1988 from the Medical College of Pennsylvania, in Philadelphia. Between 1988 and 1992, Hornig served her residency in psychiatry at the University of Vermont. Under a National Research Service Award from the National Institutes of Mental Health, she completed a postdoctoral fellowship in neuropsychopharmacology on the Depression Research Unit of the University of Pennsylvania from 1992 to 1994.


Hornig is widely recognized for her work on the role of microbial and immune factors in mental illness and neurodevelopmental disorders. In 1997, Hornig discovered a link between blood flow to brain regions regulating emotion and memory, stress hormones, and treatment failure in people with major depression, setting the stage for development of biomarkers that could match patients to the interventions most likely to help them. She is also known for her animal model research suggesting how specific gene variants (polymorphisms) present in a subset of the population may create exaggerated vulnerability to subtoxic exposures of heavy metals and other common environmental pollutants, corroborating similar findings by Jill James, Richard Deth, David Baskin, and Boyd Haley, among others.

Within the Northeast Biodefense Center, an NIAID regional center of excellence in biodefense and emerging infectious diseases, Hornig is a member of the Core Oversight Committee and the Governing Council, leading a project on immune and neuroendocrine factors in West Nile virus encephalitis.

Hornig's multidisciplinary research methods integrate data from animal models and epidemiologic studies, incorporating behavioral, neurochemical, neuroendocrine, neurostructural, molecular, immunologic and microbiologic perspectives. Hornig uses clues from animal models and epidemiologic studies to understand the neurodevelopmental responses to environmental factors during brain maturation that may trigger or amplify psychiatric conditions.

In 2004, she was elected to the President’s Council of Cornell Women, serving as Dean’s Liaison for Cornell Weill Medical College; is a member of the New York Academy of Sciences Frontiers of Science Steering Committee; serves in the Medical Reserve Corps for the NYC Department of Health and Mental Hygiene; and sits on the board of directors for The DisAbility Project in Saint Louis, Missouri.

Animal models

In the 1990s Hornig helped to develop an infection-based model of neurodevelopmental disorders such as autism, based on neonatal rat infection with Borna disease virus.[1] In a 2004 study, Hornig and her coworkers took different strains of mice, one strain predisposed to autoimmune disorders, and exposed them to mercury-preserved vaccines or to the form of mercury once present in many childhood vaccines—at the same schedule, roughly, that children were receiving around 1990. Two of the three mouse strains suffered no harm, but the autoimmune-sensitive strain developed signs consistent with autism. The onset of behavioral and brain abnormalities was associated with the appearance of autoreactive antibody deposits in the brains of the sensitive mice.[2]

A later attempt to replicate the 2004 study failed to find pervasive developmental neurotoxicity in the same mouse strain.[3] Also, while the intervals between vaccination in human infants assure nearly complete clearance of the organic species from the brain and blood, significant accumulation would be expected for the accelerated schedule in the mouse pups.[4]

According to Hornig, when several genetic markers are present, singly or in combination, children may be at much greater risk for mercury toxicity.[5] These markers may affect how efficiently the children produce the raw materials they need to detoxify, and how vulnerable their metabolic and immune system responses are to neurodevelopmental disruptions caused by mercury or other common environmental pollutants. Children whose immune systems respond inappropriately to heavy metals or other toxicants or whose metabolic machinery may be less efficient at detoxifying may have a greater vulnerability to develop autism or other neurodevelopmental conditions. These genetic markers run in families, with conditions including arthritis, colitis, chronic fatigue syndrome, lupus, celiac disease, Parkinson's Disease, and Alzheimer's.


The implications of her research findings, on the role of microbial and immune system factors in psychiatric disorders --derived from studies using animal models-- have sparked scientific debate, legislative interest, and protests from within the autism community.

Dr. Hornig has made presentations to the Institute of Medicine's Immunization Safety Review Committee, and has testified regarding the role of infections and neurotoxins before subcommittees of the United States Congress. Video presented to legislators by Hornig showed that mice belonging to the sensitive strain developed harmful repetitive behaviors following injections with thimerosal on a vaccine schedule that mimicked pediatric vaccine schedules.

Select publications

  • Mind and Immunity: Behavioral Immunology, Steven Locke, Mady Hornig-Rohan, 1983, ISBN 0-275-91400-3
  • Treatment-Resistant Mood Disorders, Jay D. Amsterdam, Mady Hornig, Andrew A. Nierenberg (editors), 2001, ISBN 0-521-59341-7


  1. ^ Hornig M, Weissenböck H, Horscroft N, Lipkin WI (1999). "An infection-based model of neurodevelopmental damage" 96 (21): 12102–7. PMID 10518583.
  2. ^ Hornig M, Chian D, Lipkin WI (2004). "Neurotoxic effects of postnatal thimerosal are mouse strain dependent". Mol Psychiatry 9 (9): 833–45. doi:10.1038/ PMID 15184908.
  3. ^ Berman RF, Pessah IN, Mouton PR, Mav D, Harry J (2007). "Low level neonatal thimerosal exposure: further evaluation of altered neurotoxic potential in SJL mice". Toxicol Sci. doi:10.1093/toxsci/kfm265. PMID 17977901.
  4. ^ Clarkson TW, Magos L (2006). "The toxicology of mercury and its chemical compounds". Crit Rev Toxicol 36 (8): 609–62. doi:10.1080/10408440600845619. PMID 16973445.
  5. ^ Autism One Conference (2005).
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Mady_Hornig". A list of authors is available in Wikipedia.
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