Sandra M. Mooney, PhD

Associate Professor of Nutrition

Sandra Mooney, PhD joined the UNC Chapel Hill Nutrition Research Institute in August 2018 as an Associate Professor of Nutrition. Her research program investigates the effect(s) of environment and genes on brain development, with a focus on prenatal alcohol exposure. Current studies use animal models to understand how nutritional needs change after alcohol exposure, thereby increasing the chances that modifying (or personalizing) nutrition will optimize growth and development. This work is supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Dr. Mooney received her Ph.D. from the University of Otago in New Zealand.

The overall theme of Dr. Mooney’s research is to understand normal brain development, how exposure to alcohol (and other drugs or experiences) disrupts this, what the behavioral outcomes are, and whether simple nutrition-based interventions can improve outcomes. Developmental exposure to ethanol profoundly affects development of the nervous system. Indeed, fetal alcohol exposure is described as the primary known cause of mental retardation, and recent estimates suggest that 2-5% of US children can be diagnosed with a Fetal Alcohol Spectrum Disorder.


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Dr. Mooney’s work has contributed to understanding that alcohol alters cell proliferation, migration, and death; all of which are critical for brain development. She has also examined the role of growth factors in these processes and shown that their expression and/or activity is altered by developmental exposure to alcohol. Ongoing work describes behavioral outcomes after acute or chronic exposure to alcohol. The acute alcohol exposure model allows understanding of how changes in anatomy, protein expression, and gene and microRNA expression in the brain align with behavioral changes. Dr. Mooney was the first to show that the timing of the alcohol exposure… 

defines the social behavior deficit, and that outcomes were sex- and age-dependent. These findings help to explain the spectrum of outcomes seen in the human population.

The lab also explores potential rescue therapy to ameliorate the effects of alcohol. Importantly, the focus is on therapies that are used after birth and could be translated into treatments for humans with Fetal Alcohol Spectrum Disorders. New studies in the design or early stages investigate the gut microbiome and structure of the gastrointestinal tract and liver.

Mooney’s Team



Proceedings of the 2019 Annual Meeting of the Fetal Alcohol Spectrum Disorders Study Group.



Alterations in the whole brain network organization after prenatal ethanol exposure.

Proceedings of the 2018 annual meeting of the Fetal Alcohol Spectrum Disorders study group.

Functional Connectivity and Metabolic Alterations in Medial Prefrontal Cortex in a Rat Model of Fetal Alcohol Spectrum Disorder: A Resting-State Functional Magnetic Resonance Imaging and in vivo Proton Magnetic Resonance Spectroscopy Study.

Quantifying Medication Exposure in Very Low Birth Weight Neonates.



Enhanced sensitivity to socially facilitating and anxiolytic effects of ethanol in adolescent Sprague Dawley rats following acute prenatal ethanol exposure.



Proceedings of the 2017 annual meeting of the Fetal Alcohol Spectrum Disorders study group.

Choline and Working Memory Training Improve Cognitive Deficits Caused by Prenatal Exposure to Ethanol.

Heterogeneity of p53 dependent genomic responses following ethanol exposure in a developmental mouse model of fetal alcohol spectrum disorder.

The Role of CREB, SRF, and MEF2 in Activity-Dependent Neuronal Plasticity in the Visual Cortex.



Prenatal Ethanol Exposure and Whisker Clipping Disrupt Ultrasonic Vocalizations and Play Behavior in Adolescent Rats.

Corrigendum to “Docosahexaenoic acid partially ameliorates deficits in social behavior and ultrasonic vocalizations caused by prenatal ethanol exposure” [Behav. Brain Res. 286 (2015) 201-211].

Acute prenatal exposure to ethanol on gestational day 12 elicits opposing deficits in social behaviors and anxiety-like behaviors in Sprague Dawley rats.