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Mary Ann Wilson, Ph.D.

Photo of Dr. Mary Ann Wilson, Ph.D.

Associate Professor of Neurology

Background

Dr. Wilson received her bachelor's of arts in both art and physiology from the University of California at Berkeley before coming to Johns Hopkins for a doctoral degree in biochemistry, cellular and molecular biology, which she received in 1990. She held post-doctoral fellowships at Hopkins’ Department of Neuroscience and Kennedy Krieger Institute's neuroscience lab before joining the research faculty at Kennedy Krieger Institute in 1994.

Dr. Wilson was elected to Phi Beta Kappa at UC-Berkeley in 1982, and received her degree in physiology with honors. She was awarded a pre-doctoral fellowship in systems and integrative biology at UC-Berkley in 1982, and was awarded a pre-doctoral fellowship in biochemistry, cellular and molecular biology at Hopkins in 1983.

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Titles

  • Associate Professor of Neurology
  • Associate Professor of Neuroscience

Departments / Divisions

Education

Degrees

  • Ph.D., Johns Hopkins University School of Medicine (Maryland) (1990)

Additional Training

The Johns Hopkins University School of Medicine, Baltimore, MD, 1994, Neurology and Neuroscience

Research & Publications

Research Summary

Excitatory amino acids are important neurotransmitters in the developing brain, but excess stimulation of EAA receptors can injure nerve tissue. Excitatory amino acids contribute to many forms of acute and chronic neuronal injury including hypoxia/ischemia, status epilepticus, trauma and neurodegenerative diseases such as Huntington’s and Parkinson’s disease. The developing brain is particularly vulnerable to excitotoxic injury, due in part to the expression of immature glutamate receptors.

Dr. Wilson studies the developing brain’s responses to excitotoxic injury and toxins, in order to develop strategies to prevent or reduce neuronal damage. She works to relate changes in the expression of glutamate receptors and other genes to changes in the vulnerability of particular cell groups to injury. Lead is a widespread environmental contaminant that is toxic to nerve tissue.

Lead poisoning constitutes a major medical issue worldwide, including numerous US cities such as Baltimore. Despite efforts to reduce the amount of lead in the environment, lead poisoning is common among poor urban children; approximately 5% of the children tested in Baltimore from 1996 to 1998 suffered blood lead levels greater than 20 mg/dl.

Currently one of the things Dr. Wilson is working on is a project to evaluate the hypothesis that glutamate receptors have a critical role in the long-lasting effects of lead exposure during brain development. The "Barrel Field" in the primary somatosensory cortex of rodents is used as a model system for these studies. Rodents have distinct clusters of neurons in the cerebral cortex, called "barrels", that process sensory input from the whiskers. Dr. Wilson and her colleagues use this model to evaluate alterations in cortical development and plasticity caused by neonatal lead exposure.

Selected Publications

  1. Ischemia-induced neuroinflammation is associated with disrupted development of oligodendrocyte progenitors in a model of periventricular leukomalacia. Falahati S, Breu M, Waickman AT, Phillips AW, Arauz EJ, Snyder S, Porambo M, Goeral K, Comi AM, Wilson MA, Johnston MV, Fatemi A. Dev Neurosci. 2013;35(2-3):182-96. doi: 10.1159/000346682. Epub 2013 Feb 27. PMID: 23445614
  2. Serum levels of neuron-specific ubiquitin carboxyl-terminal esterase-L1 predict brain injury in a canine model of hypothermic circulatory arrest. Arnaoutakis GJ, George TJ, Wang KK, Wilson MA, Allen JG, Robinson CW, Haggerty KA, Weiss ES, Blue ME, Talbot CC Jr, Troncoso JC, Johnston MV, Baumgartner WA. J Thorac Cardiovasc Surg. 2011 Oct;142(4):902-910.e1. doi: 10.1016/j.jtcvs.2011.06.027. PMID: 21924148
  3. In vivo magnetization transfer MRI shows dysmyelination in an ischemic mouse model of periventricular leukomalacia. Fatemi A, Wilson MA, Phillips AW, McMahon MT, Zhang J, Smith SA, Arauz EJ, Falahati S, Gummadavelli A, Bodagala H, Mori S, Johnston MV. J Cereb Blood Flow Metab. 2011 Oct;31(10):2009-18. doi: 10.1038/jcbfm.2011.68. Epub 2011 May 4. PMID: 21540870
  4. Treatment advances in neonatal neuroprotection and neurointensive care. Johnston MV, Fatemi A, Wilson MA, Northington F. Lancet Neurol. 2011 Apr;10(4):372-82. doi: 10.1016/S1474-4422(11)70016-3. Review. PMID: 21435600
  5. Sex-specific activation of cell death signalling pathways in cerebellar granule neurons exposed to oxygen glucose deprivation followed by reoxygenation. Sharma J, Nelluru G, Wilson MA, Johnston MV, Hossain MA. ASN Neuro. 2011 Apr 7;3(2). pii: e00056. doi: 10.1042/AN20100032. PMID: 21382016

Activities & Honors

Memberships

  • Barrels Society: , 2003
    Organizing Committee member, 2003-2004 and 2006-2007
  • Local Organizing Committee, Barrels XVIII, 2005
  • Serotonin Club, 1986
    Member
  • Session Chair, Barrels XVII, 2004
  • Society for Neuroscience, 1986
    Member

Professional Activities

  • Teaching Assistant, University of California, 1982 - 1983
    Dept. of Physiology and Anatomy

Videos & Media

Lectures and Presentations

  • Neonatal lead exposure impairs morphologic plasticity after whisker follicle ablation.
    Barrels XVI , New Orleans, Louisiana (01/01/2003)
  • Effects of Neonatal Lead Exposure on the Development and Plasticity of Rat Somatosensory Cortex.
    Pediatric Neurology Grand Rounds , Baltimore, Maryland (01/14/2004)
    Johns Hopkins University School of Medicine
  • Neonatal lead exposure impairs morphologic plasticity after whisker follicle ablation.
    Barrel Cortex Meeting, EPFL , Lausanna, Switzerland (02/01/2004)
  • Activity-dependent Expression of the Inducible Transcription Factor Egr1 in Developing Barrel Cortex.
    Neuroscience Graduate Program & Physiology Graduate Program Seminar Series , Syracuse, New York (12/17/2004)
    SUNY Upstate Medical University
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