Welcome to the Schwarz Lab

Research Interests:

Our lab examines how immune activation influences the brain and behavior throughout the lifespan. 

Many neuropsychiatric disorders have been linked to early-life immune activation or immune dysregulation, yet it is not known how activation of the immune system early in life can program brain and behavior.  There is constant communication between the brain and the immune system that can influence the brain and behavior. 

During certain times in life, we hypothesize that immune activation can change the trajectory of the immune cells in the periphery and in the brain to influence behavior long-term. 

Current Lab Members:

Jaclyn M. Schwarz, Ph.D. – Principal Investigator

Nicole A. Haas, M.S. – Laboratory Manager

Janace Gifford, Ph.D. - Postdoctoral Researcher

Mary Beth Bielicki – Graduate Research Assistant

Elise Lemanski – Graduate Research Assistant

Elizabeth McAuley – Graduate Research Assistant, 4+1 Neuroscience Master’s Program

Undergraduate Research Assistants – Megan Muench, Nicola Habash, Jenna Pluchino, Daria Willis

Former Lab Members: 

Morgan Sherer​, Ph.D. (postdoctoral researcher at Johns Hopkins Bloomberg School of Public Health), Alexandra Turano, Ph.D.  (postdoctoral researcher at Utah State University), Rita Patel, M.S., Brittany F. Osborne, Ph.D. (postdoctoral researcher at CHOP/UPenn), Julie Gomez, M.S. (medical student at Sidney Kimmel Medical College at Jefferson), Sarah Beamish (Graduate Researcher at University of Wisconsin, Milwaukee), Jennifer Lawrence (Graduate Researcher at Washington University in St. Louis), Caitlin Posillico (Graduate Researcher at University of Michigan), Laurne Terasaki (medical student at Virginia Commonwealth University Medical School), and Jasmine Caulfield (Graduate Researcher at Penn State University).

If you are interested in the brain, development, and behavior, consider joining our lab and working on one of the projects listed below.

​Research Project #1:  How does early-life immune dysregulation result in the emergence of learning disorders? 

Funding:  NIH R01MH106553

Dysregulation of the immune system during childhood increases the risk for mental health disorders such as autism spectrum disorders, schizophrenia and pervasive developmental disorders. Notably, these disorders exhibit a strong sex bias, with males being more vulnerable to these developmental disorders than females. Microglia are the primary immune cells of the brain that respond to immune dysregulation. Microglia-neuron communication is necessary for the proper formation of neural circuits that support the emergence and long-term maintenance of cognitive function.  We have found that immune activation during juvenile brain development, produces deficits in the emergence of hippocampal-dependent learning days later. Our data suggest that sex-specific dysregulation in microglia-neuron communication may disrupt the development of neural circuits in the hippocampus following immune activation or dysregulation. These changes may be a key mechanism underlying sex differences in vulnerability to developmental and neuropsychiatric disorders caused by early-life immune activation.

Research Project #2: How do changes in the immune system during pregnancy contribute to postpartum mood disorders?​​

Funding: NIH R21MH122862

Postpartum depression affects around 15% of mothers, and suicide associated with postpartum depression is one of the leading causes of maternal death in first world countries. Key risk factors for postpartum depression include low social support, low socioeconomic status, unemployment, and negative life events during pregnancy. All of these risk factors have a common theme: psychological, social, or physical resource scarcity, suggesting that the LBN paradigm could provide a novel and naturalistic model for examining its effects on the risk of postpartum depression using rodents. Pre-clinical research on post-partum depression (PPD) has until now focused largely on the contributions of sex hormones and psychosocial stress, with very little focus on the impact of inflammation despite the growing body of evidence that inflammation may contribute to depression. The current project aims to explore whether using chronic limited bedding and nesting as a stress during and following pregnancy provides more robust, chronic changes in anhedonic behavior, and whether these are associated with changes in inflammatory state caused by either the peripartum period itself, or in combination with stress.

Research Project #3:  Impact of prenatal Zika virus infection on brain development and later-life behaviorResearch Project #4:  Role of small bacterial fragments from the microbiome in brain-immune communication.

Funding:  NIH R21HD096309

Collaboration with Dr. Mark Parcells (Department of Animal and Food Sciences)

Zika virus (ZIKV), a mosquito-borne flavivirus, has been associated with microcephaly and other neurological disorders in infants born to infected mothers. Despite being declared an international emergency by the World Health Organization, comparatively very little is known about the pathogenesis, mechanisms, or behavioral consequences of maternal ZIKV infection in the offspring. Our lab is interested in developing a working animal model to answer some of these questions. Here, we use a rat model of prenatal ZIKV infection to measure the level of infectivity, as well as the rate of viral clearance in both the mother and her pups. We examine various aspects of brain development in pups, including cortical thickness, microglia morphology, apoptosis, and neurogenesis. Further, we use this model to investigate the impact of prenatal ZIKV infection on hippocampal and non-hippocampal dependent learning as well as motor learning in the juvenile and adult offspring. Given that pregnancy is associated with significant immunomodulation, we are also interested in the role that pregnancy has on the impact of ZIKV infection, therefore we compare viral infectivity between both pregnant and non-pregnant female rats.

Research Project #4:  Role of small bacterial fragments from the microbiome in brain-immune communication.

Collaboration with Dr. Catherine L. Grimes (Department of Chemistry & Biochemistry)

Unlike most of the body's organs, the brain exists behind a blood-brain barrier designed to minimize the passage of cells and pathogens into delicate neural tissue. Yet, our body is colonized with a vast array of commensal bacteria known as the microbiome, and a plethora of growing data highlight an important relationship between the composition of the microbiome and various brain disorders including Alzheimer's disease, depression and autism. The molecular mechanisms of this intriguing relationship are relatively unknown. Our proposed experiments will determine whether the small cell wall metabolites produced by these bacteria gain access to the brain, and if they do, what do they do there? To date, it's been assumed that communication between the microbiome and the brain is exclusively indirect, occurring via communication with the endocrine, immune and autonomic nervous systems. We hypothesize, rather, that small carbohydrate fragments derived from the cell wall of the microbiota can translocate to the brain thereby directly and continuously influencing brain function and health.

Undergraduate students in Neuroscience, Psychology and Biology: 

If you are interested in joining the lab, send an updated resume, unofficial transcript and the following  application:  Schwarz Lab Undergraduate Interview form.docx to Dr. Schwarz at jschwarz@udel.edu.​

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