Elinor Sullivan

 

Assistant Professor, Department of Human Physiology
Member, ION

Ph.D. Oregon Health and Science University
 

elinors@uoregon.edu
Lab Website
Office: 
Phone: 485-215-0227

 

Research Interests: 

Overview: 

Elinor Sullivan’s teaching focus is in the areas of nutrition, endocrinology, and neurobiology.

Dr. Sullivan’s research focuses on examining the influence of maternal metabolic state and dietary environment on offspring behavioral regulation, with an emphasis on behaviors that relate to mental health and behavioral disorders including autism spectrum disorders, attention deficit hyperactivity disorder, anxiety, and depression.

Her areas of expertise include behavioral neuroscience, with training and expertise in human and nonhuman primate behavior, brain development, developmental programming, maternal nutrition, and neurodevelopmental disorders.

Dr. Sullivan received her Ph.D. in Physiology from Oregon Health and Science University. She received her postdoctoral training at the University of California San Francisco and Oregon Health and Science University. Prior to coming to the University of Oregon, Dr. Sullivan was an Assistant Professor in the Biology Department at the University of Portland. Dr. Sullivan is currently an Assistant Professor in the Divisions of Neuroscience and Cardiometabolic health at the Oregon National Primate Research Center. She joined the UO Department of Human Physiology in 2017.

Dr. Sullivan has received research grants from the National Institute of Health, the Bill and Melinda Gates Foundation, the Murdock Charitable Trust, and the Obesity Society.

RECENT PUBLICATIONS

Related Articles

Neuroinflammation as a risk factor for attention deficit hyperactivity disorder.

Pharmacol Biochem Behav. 2019 07;182:22-34

Authors: Dunn GA, Nigg JT, Sullivan EL

Abstract
Attention Deficit Hyperactivity Disorder (ADHD) is a persistent, and impairing pediatric-onset neurodevelopmental condition. Its high prevalence, and recurrent controversy over its widespread identification and treatment, drive strong interest in its etiology and mechanisms. Emerging evidence for a role for neuroinflammation in ADHD pathophysiology is of great interest. This evidence includes 1) the above-chance comorbidity of ADHD with inflammatory and autoimmune disorders, 2) initial studies indicating an association with ADHD and increased serum cytokines, 3) preliminary evidence from genetic studies demonstrating associations between polymorphisms in genes associated with inflammatory pathways and ADHD, 4) emerging evidence that early life exposure to environmental factors may increase risk for ADHD via an inflammatory mechanism, and 5) mechanistic evidence from animal models of maternal immune activation documenting behavioral and neural outcomes consistent with ADHD. Prenatal exposure to inflammation is associated with changes in offspring brain development including reductions in cortical gray matter volume and the volume of certain cortical areas -parallel to observations associated with ADHD. Alterations in neurotransmitter systems, including the dopaminergic, serotonergic and glutamatergic systems, are observed in ADHD populations. Animal models provide strong evidence that development and function of these neurotransmitters systems are sensitive to exposure to in utero inflammation. In summary, accumulating evidence from human studies and animal models, while still incomplete, support a potential role for neuroinflammation in the pathophysiology of ADHD. Confirmation of this association and the underlying mechanisms have become valuable targets for research. If confirmed, such a picture may be important in opening new intervention routes.

PMID: 31103523 [PubMed - indexed for MEDLINE]

Related Articles

Perinatal Nutrition and Programmed Risk for Neuropsychiatric Disorders: A Focus on Animal Models.

Biol Psychiatry. 2019 01 15;85(2):122-134

Authors: DeCapo M, Thompson JR, Dunn G, Sullivan EL

Abstract
Maternal nutrition is critically important for fetal development. Recent human studies demonstrate a strong connection between diet during pregnancy and offspring risk for neuropsychiatric disorders including depression, anxiety, and attention-deficit/hyperactivity disorder. Animal models have emerged as a crucial tool for understanding maternal nutrition's contribution to prenatal programming and the later development of neuropsychiatric disorders. This review highlights preclinical studies examining how maternal consumption of the three macronutrients (protein, fats, and carbohydrates) influence offspring negative-valence behaviors relevant to neuropsychiatric disorders. We highlight the translational aspects of animal models and so examine exposure periods that mirror the neurodevelopmental stages of human gestation. Because of our emphasis on programmed changes in neurobehavioral development, studies that continue diet exposure until assessment in adulthood are not discussed. The presented research provides a strong foundation of preclinical evidence of nutritional programming of neurobehavioral impairments. Alterations in risk assessment and response were observed alongside neurodevelopmental impairments related to neurogenesis, synaptogenesis, and synaptic plasticity. To date, the large majority of studies utilized rodent models, and the field could benefit from additional study of large-animal models. Additional future directions are discussed, including the need for further studies examining how sex as a biological variable affects the contribution of maternal nutrition to prenatal programming.

PMID: 30293647 [PubMed - indexed for MEDLINE]