Thomas W. Bastian, PhD

Assistant Professor, Department of Pediatrics

Thomas W. Bastian

Contact Info

Office Phone 612-626-2961

Mailing Address:
Academic Office Building
2450 Riverside Ave S AO-401
Minneapolis, MN 55454

Fellowship in Nutritional Neuroscience, University of Minnesota, Minneapolis, MN

PhD, Integrated Biosciences, University of Minnesota-Duluth, Duluth, MN

BS, Biochemistry/Molecular Biology and Chemistry, University of Minnesota-Duluth, Duluth, MN


Thomas Bastian, PhD, is an Assistant Professor of Pediatrics in the Division of Neonatology. Dr. Bastian’s research focuses on understanding the metabolic regulation of both normal and pathogenic brain development. His lab is particularly interested in the basic neurodevelopmental biology of micronutrients (e.g., iron, zinc, copper, etc) and how developing brain cells metabolically adapt to disruptions to nutrient perturbations. Dr. Bastian’s research is currently funded by the National Institutes of Health and the Department of Pediatrics.


Neurodevelopment, metabolism, cell culture

Awards & Recognition

  • Basic Science Paper of the Year (Assistant Professor), Department of Pediatrics, University of Minnesota (2020)


Research Summary/Interests

Research in the Bastian Lab focuses on uncovering the cellular/molecular mechanisms by which specific nutrients regulate brain development. We have a particular interest in metabolic interactions among micronutrients (e.g., iron, iodine, copper, and zinc) and metabolic regulators (e.g., thyroid hormone), which are directly involved in cellular energy metabolism in the developing brain. Our goal is to understand how these interactions contribute to proper brain development. We use primary neuron culture and in vivo transgenic approaches to manipulate cellular levels of micronutrients (and other metabolic pathways) in developing brain cells, allowing us to study interactions between cellular metabolic processes that are critical for neurodevelopment. This line of research is also clinically relevant as early-life micronutrient deficiencies are common and cause abnormal neurodevelopment in humans.

Currently, our main research focus is on how early-life iron deficiency and subsequent iron repletion alter mitochondrial energy metabolism in developing neurons and how this contributes to the neurobehavioral deficits that persist into adulthood. A second goal is to understand how intracellular iron storage and utilization is regulated in developing neurons.


Bastian TW, Rao R, Tran PV, Georgieff MK. (2020) The Effects of Early-Life Iron Deficiency on Brain Energy Metabolism. Neurosci Insights. 15, 2633105520935104

Bastian TW, von Hohenberg WC, Georgieff MK, Lanier LM (2019) Chronic energy depletion due to iron deficiency impairs dendritic mitochondrial motility during hippocampal neuron development. J Neurosci. 39(5):802-813

Bastian TW, von Hohenberg WC, Mickelson DJ, Lanier LM, Georgieff MK (2016) Iron deficiency impairs developing hippocampal neuron gene expression, energy metabolism and dendrite complexity. Dev Neurosci 38: 264–76

Bastian TW, Prohaska JR, Georgieff MK, Anderson GW (2010) Perinatal iron and copper deficiencies alter neonatal rat circulating and brain thyroid hormone concentrations. Endocrinology 151:4055-4065

Complete list of publications in My Bibliography: