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Mary C. McKenna, PhD

Academic Title:

Professor

Primary Appointment:

Pediatrics

Administrative Title:

Department APT Chair

Additional Title:

Professor, Department of Pediatrics and Program in Neuroscience

Location:

BRB, 13-019

Phone (Primary):

(410) 706-1990 - office

Phone (Secondary):

(410) 706-4222 - lab

Fax:

(410) 706-2611

Education and Training

Education

1968    B.A.     University of Maryland, College Park, MD; Major, English, Minor, History

1979    Ph.D.   University of Maryland, College Park, MD.; Major: Nutritional        Biochemistry;

                        Minor: Biostatistics;

Postgraduate Training

1979-1982      Staff Fellow, Nutritional Biochemistry Section, Laboratory of Nutrition and Endocrinology, NIADDK, NIH, Bethesda, MD, Mentor: John G. Bieri, Ph.D.

1982               Guest Worker, Pediatric Metabolism Branch, Laboratory of Cellular and Developmental Biology, NAIDDK, NIH, Bethesda, MD. mentor: Van S. Hubbard, M.D., Ph.D.

1990-1993      Guest Worker, Laboratory of Mathematical Biology, NCI, NIH, Bethesda, MD. Mentor: Loren Zech, M.D.

Biosketch

Research in Dr. McKenna's lab has focused on questions related to developmental brain injury, regulation of key enzymes and the regulation of energy metabolism in astrocytes and synaptic terminals for the past 39 years. In 1993 with several other investigators, she was a founder of the series of International Conferences on Brain Energy metabolism, the 14th of which will be held in October 2022. Dr. McKenna has internationally recognized expertise in the field of brain energy metabolism and currently serves as an editor for several journals in this field. Studies from her lab have significantly advanced the fundamental understanding of the complexity of metabolic compartmentation, and both neuronal and astrocytic metabolism in brain.

The primary focus of the current studies in Dr. McKenna's lab is determining acute metabolic alterations in brain that contribute to secondary energy failure and long term damage after neonatal hypoxic-ischemic injury. Results reveal a close relationship between the extent of oxidative stress and impaired cerebral energy metabolism in early periods of recovery after HI. Four studies demonstrate that treatment with acetyl-L-carnitine (ALCAR) after injury decreases lesion size, protects mitochondrial function and improves motor skills and memory.

Dr. McKenna's studies utilize ex vivo 13C-NMR spectroscopy to determine the effects of injury and neuroprotection on brain metabolism. This powerful technique can determine alterations in neuronal metabolism, neuron --> astrocyte trafficking, astrocyte metabolism, and astrocyte --> neuron trafficking. 13C-NMR spectroscopy can be used to quantify newly synthesized compounds in brain and to identify cell specific pathways of metabolism impaired by brain injury. Current studies focus on the cerebellum which is understudied in HI and includes assessing short and long term behavioral outcomes in the postnatal day 10 rat pup model of HI in term infants. Studies provide evidence that protecting energy metabolism can protect the brain from injury after neonatal HI and pediatric TBI.

Research/Clinical Keywords

Brain energy metabolism, developmental brain injury and neuroprotection, neonatal hypoxia-ischemia (HI), 1H and 13C-NMR spectroscopy, neurotransmitter synthesis, regulation of brain enzymes, neuron-->astrocyte and astrocyte-->neuron metabolic trafficking in brain, glutamate, glutamine, astrocytes, synaptic terminals

Highlighted Publications

McKenna MC (2007) The glutamate-glutamine cycle is not stoichiometric: fates of glutamate in brain. J Neurosci Res 85(15):3347-3358. DOI: 10.1002/jnr.21444.

Scafidi S, Fiskum G, Lindauer SL, Bamford P, Shi D, Hopkins IB, McKenna, MC. (2010) Metabolism of the neuroprotective compound acetyl-L-carnitine for energy metabolism and neurotransmitter synthesis in the immature rat brain. J Neurochem 114(3):820-831. PMID: 20477950

Demarest T, Waddell J, McKenna MC, Schuh R, Fiskum G. (2016) Sex-dependent mitochondrial respiratory impairment and oxidative stress in a rat model of neonatal hypoxic ischemic encephalopathy. J Neurochem 137(5):714-729. PMCID: PMC4876982

Xu S, Waddell J, Zhu W, Shi D, Marshall AD, McKenna MC, Gullapalli RP. In vivo longitudinal proton magnetic resonance spectroscopy on neonatal hypoxic-ischemic brain injury: neuroprotective effects of acetyl-L-carnitine. Magn Reson Med. 74:1530-1542. PMCID: PMC4452442

Ferriera GC, Karimi AJ, Waddell J, McKenna MC. (2021) Metabolism of [1,6-13C]glucose in the cerebellum of 18-day-old-rats: Comparison with cerebral metabolism. J Neurochem. 157(6):1946-1962. DOI: 10.1111/jnc.15326.