Mary Ann Wilson, Ph.D.

Mary Ann Wilson, Ph.D.'s picture
Research Scientist, Kennedy Krieger Institute

Kennedy Krieger Institute
707 N. Broadway
Baltimore, MD 21205
Phone: (443) 923-2691
Lab: (443) 923-2694

Dr. Mary Ann Wilson is a research scientist at the Kennedy Krieger Institute and an associate professor in the Departments of Neurology and Neuroscience at the Johns Hopkins University School of Medicine.

Biographical Sketch: 

Dr. Wilson received her bachelor 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 developmental 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-Berkely in 1982, and was awarded a pre-doctoral fellowship in biochemistry, cellular and molecular biology at Hopkins in 1983.

Research Summary: 

Neurodevelopmental disorders such as cerebral palsy and autism are common chronic childhood disorders with no effective cure. Half a million children under the age of 18 in the United States have cerebral palsy, and one in 6 children have some form of developmental disability. In term infants that suffer asphyxia at birth, low oxygen levels and low blood flow can cause hypoxic-ischemic encephalopathy, which is a major cause of cerebral palsy and related disabilities. Dr. Wilson’s research is focused on reducing brain damage in infants exposed to perinatal hypoxia-ischemia. Therapeutic hypothermia is the first intervention to reduce brain injury in term infants after perinatal asphyxia, but protection is typically incomplete and rates of mortality and severe disability remain high. There remains a critical need for complementary therapies that improve neuroprotection and address the negative effects of hypothermia and rewarming.

Dr. Wilson investigates molecular mechanisms of hypoxic ischemic injury in the developing brain and neuroprotective effects of drugs, hypoxic preconditioning, and hypothermia. She has investigated how changes in gene expression after a brief period of hypoxia reduce the vulnerability of the brain to a later, more severe HI insult. She also studies sex differences in brain injury mechanisms that are triggered by hypoxic ischemic injury in neonatal mice and has shown that there are sex-specific differences in the neuroprotective effects of some therapeutic interventions. Dr. Wilson’s current work investigates the neuroprotective mechanisms engaged by hypothermia in neonates, with the goal of developing complementary therapies that enhance hypothermic neuroprotection.

Dr. Wilson also collaborates with Dr. William Baumgartner and colleagues to study brain injury after hypothermic circulatory arrest (HCA). This research uses an animal model of this surgical intervention, which is used for complex repairs to the heart or major vessels in infants and adults. These studies have revealed inflammatory as well as apoptotic mechanisms that are activated after hypothermic circulatory arrest and have also identified serum biomarkers that can be used to detect brain injury early in the postoperative period. Studies in collaboration with Drs. Kannan Rangaramanujam and Sujatha Kannan recently showed that dendrimer nanoparticles can be used to deliver therapy to injured neurons and activated microglia after hypothermic circulatory arrest. This therapeutic approach holds great promise for prevention of brain injury after hypothermic circulatory arrest; Dr. Wilson and her colleagues are also investigating dendrimer nanotherapy for treatment of neonatal hypoxic-ischemic brain injury.

Research Publications:

Zhang F, Trent Magruder J, Lin YA, Crawford TC, Grimm JC, Sciortino CM, Wilson MA, Blue ME, Kannan S, Johnston MV, Baumgartner WA, Kannan RM (2017). Generation-6 hydroxyl PAMAM dendrimers improve CNS penetration from intravenous administration in a large animal brain injury model. J Control Release. 249, 173-182. Abstract
Grimm JC, Magruder JT, Wilson MA, Blue ME, Crawford TC, Troncoso JC, Zhang F, Kannan S, Sciortino CM, Johnston MV, Kannan RM, Baumgartner WA (2016). Nanotechnology Approaches to Targeting Inflammation and Excitotoxicity in a Canine Model of Hypothermic Circulatory Arrest-Induced Brain Injury. Ann Thorac Surg. 102(3), 743-50. Abstract
Blue ME, Wilson MA, Beaty CA, George TJ, Arnaoutakis GJ, Haggerty KA, Jones M, Brawn J, Manmohan S, Lange MS, Johnston MV, Baumgartner WA, Troncoso JC (2014). Brain injury in canine models of cardiac surgery. J Neuropathol Exp Neurol. 73(12), 1134-43. Abstract
Mishra MK, Beaty CA, Lesniak WG, Kambhampati SP, Zhang F, Wilson MA, Blue ME, Troncoso JC, Kannan S, Johnston MV, Baumgartner WA, Kannan RM (2014). Dendrimer brain uptake and targeted therapy for brain injury in a large animal model of hypothermic circulatory arrest. ACS Nano. 8(3), 2134-47. Abstract
Falahati S, Breu M, Waickman AT, Phillips AW, Arauz EJ, Snyder S, Porambo M, Goeral K, Comi AM, Wilson MA, Johnston MV, Fatemi A (2013). Ischemia-induced neuroinflammation is associated with disrupted development of oligodendrocyte progenitors in a model of periventricular leukomalacia. Dev Neurosci. 35(2-3), 182-96. Abstract
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 (2011). Serum levels of neuron-specific ubiquitin carboxyl-terminal esterase-L1 predict brain injury in a canine model of hypothermic circulatory arrest. J Thorac Cardiovasc Surg. 142(4), 902-910.e1. Abstract
Fatemi A, Wilson MA, Phillips AW, McMahon MT, Zhang J, Smith SA, Arauz EJ, Falahati S, Gummadavelli A, Bodagala H, Mori S, Johnston MV (2011). In vivo magnetization transfer MRI shows dysmyelination in an ischemic mouse model of periventricular leukomalacia. J Cereb Blood Flow Metab. 31(10), 2009-18. Abstract
Allen JG, Weiss ES, Wilson MA, Arnaoutakis GJ, Blue ME, Talbot CC Jr, Jie C, Lange MS, Troncoso JC, Johnston MV, Baumgartner WA (2010). Hawley H. Seiler Resident Award. Transcriptional profile of brain injury in hypothermic circulatory arrest and cardiopulmonary bypass. Ann Thorac Surg. 89(6), 1965-71. Abstract
Weiss ES, Wang KK, Allen JG, Blue ME, Nwakanma LU, Liu MC, Lange MS, Berrong J, Wilson MA, Gott VL, Troncoso JC, Hayes RL, Johnston MV, Baumgartner WA (2009). Alpha II-spectrin breakdown products serve as novel markers of brain injury severity in a canine model of hypothermic circulatory arrest. Ann Thorac Surg. 88(2), 543-50. Abstract
Gustavsson M, Mallard C, Vannucci SJ, Wilson MA, Johnston MV, Hagberg H (2007). Vascular response to hypoxic preconditioning in the immature brain. J Cereb Blood Flow Metab. 27(5), 928-38. Abstract
Comi AM, Highet BH, Mehta P, Hana Chong T, Johnston MV, Wilson MA (2006). Dextromethorphan protects male but not female mice with brain ischemia. Neuroreport. 17(12), 1319-22. Abstract
Hagberg H, Wilson MA, Matsushita H, Zhu C, Lange M, Gustavsson M, Poitras MF, Dawson TM, Dawson VL, Northington F, Johnston MV (2004). PARP-1 gene disruption in mice preferentially protects males from perinatal brain injury. J Neurochem. 90(5), 1068-75. Abstract
Matsushita H, Johnston MV, Lange MS, Wilson MA (2003). Protective effect of erythropoietin in neonatal hypoxic ischemia in mice. Neuroreport. 14(13), 1757-61. Abstract
Nakajima W, Ishida A, Lange MS, Gabrielson KL, Wilson MA, Martin LJ, Blue ME, Johnston MV (2000). Apoptosis has a prolonged role in the neurodegeneration after hypoxic ischemia in the newborn rat. J Neurosci. 20(21), 7994-8004. Abstract
Wilson MA, Johnston MV, Goldstein GW, Blue ME (2000). Neonatal lead exposure impairs development of rodent barrel field cortex. Proc Natl Acad Sci U S A. 97(10), 5540-5. Abstract

Other Publications:

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