My overall research interest lies in investigating typical brain development as it relates to adult behavior, and how common early-life experiences can alter developmental trajectories. Common early-life factors such as diet and stress can impact offspring brain and behavior for an entire lifespan – a phenomenon termed “perinatal programming.” In my graduate work, I discovered that perinatal dietary choline supplementation “reprogrammed” the developing immune system to be anti-inflammatory, neuroprotective, and protective against cognitive deficits after an adult inflammatory assault. In my postdoctoral work, I have focused on striatal-dependent behaviors affected by prenatal stress. I am motivated by investigating how neurodevelopment can be altered by early life events.
University of Iowa, 2020 - present
As a postdoc in Dr. Hanna Stevens's lab, I'm currently assessing the role of IL-6 in prenatal stress-induced striatal overgrowth. Autism spectrum disorder (ASD) is linked to the striatum (reviewed in Goodman et al., 2014). Behaviors associated with ASD, such as communicative impairments and repetitive behaviors, have been tied to striatal alterations (reviewed in Goodman et al., 2014). Previous work in mouse models for the study of ASD has shown increases in striatal volume (Kumar et al., 2018), alterations in striatal function, and striatal-dependent learning deficits (Grissom et al., 2018). These findings are consistent with human studies indicating an increased striatum volume (Qiu et al., 2016; Estes et al., 2011; Hazlett et al., 2009) and impairments in striatal-dependent learning in patients with ASD (Goh & Peterson, 2012). However, little is understood about the mechanisms behind the development of this striatal overgrowth with cell-type specificity. Medium spiny neurons (MSNs) in the striatum have been implicated in striatal-dependent learning (De Corte et al., 2019) – a behavior impaired in ASD (Goh & Peterson, 2012). Despite the clear link between striatum and ASD, little research has been devoted to changes in striatal MSNs in ASD-relevant mouse models, as well as the embryonic origins of striatal abnormalities with respect to this cell type.
ASD incidence has been powerfully linked with perinatal stress in humans (Class et al., 2014; Walder et al., 2014; Roberts et al., 2016). Prenatal stress also leads to maternal immune activation (Ross et al., 2019). Maternal IL-6 has additionally been linked to brain overgrowth, among other ASD-related alterations in brain and behavior (Gumusoglu et al., 2017; Smith et al., 2007; Bonnet-Brilhault et al., 2018). Preliminary work in Dr. Hanna Stevens’ lab has shown that prenatal stress increases the number of MSNs in mouse striatum across developmental timepoints, consistent with volumetric increases found in another ASD model (Kumar et al., 2018). However, a mechanistic link between prenatal stress and MSNs throughout development has not been explored. I hypothesize that IL-6 is sufficient for and is a necessary component of the stress-induced increase in MSNs in the striatum throughout the lifespan. I am currently using unbiased stereology, next generation sequencing, and in utero intracerebroventricular injections to answer these questions.
Selected publications and presentations:
"MSNs and Prenatal Stress," (2020). INSPIRE seminar presentation.
Maurer, S. V. (2022, November). Maternal stress: sex- and age-specific outcomes. Seminar presenter at the biology department of Hope College, virtual.
Maurer, S. V., Evans, M. M., & Stevens, H. E. (2022, October). Maternal chronic IL-6 impacts striatal-dependent behavior in a sex, age, and experience dependent manner. Pitch presentation at the annual meeting of the U.S. DOHaD Society, Minneapolis, MN.
Maurer, S. V. (2022, September). Maternal stress and IL-6: shared and distinct offspring outcomes. Organizer and presenter for the September 2022 Pediatric Neuroscience Collaborative (PNC) seminar at Johns Hopkins University. Virtual.
Duke University, 2014 - 2020
As a graduate student in Dr. Christina L. Williams's lab, I studied the lifelong neuroprotective actions of prenatal choline, specifically with relation to its anti-inflammatory properties. Inflammatory events during fetal life can “program” neuroimmune cells – specifically, microglia – to overreact to adult immune challenges (Bilbo, 2013), which subsequently also leads to cognitive deficits and mental illness in adulthood (Graciarena, Depino, & Pitossi, 2010; Patterson, 2002). Neuroinflammation research is currently focused on its causes within the Western lifestyle, such as high-fat diet, stress, and air pollution (Pistell et al., 2010; Black & Garbutt, 2002; Calderόn-Garcidueñas et al., 2004). However, for pregnant women in locations with low-nutrient foods, with unavoidable stress, and without the means to simply move away from air pollution, pinpointing the cause behind neuroinflammation and its cognitive effects does not alone provide a solution for their offspring. If supplementation with a low-cost nutrient could prevent neuroinflammation, or at the very least the long-term consequences of it, pregnant women in these situations could avoid the mental health and neurobiological consequences of a neuroinflammatory milieu for their offspring.
Dietary choline supplementation in adulthood can be beneficial to memory and neurogenesis (Tabassum & Haider, 2016). Additionally, cholinergic agonists, such as choline, have been shown to be anti-inflammatory (Terrando et al., 2011). Though the anti-inflammatory aspect of choline and how it impacts memory has been documented, this phenomenon has only been observed acutely in adulthood.
Prenatal choline supplementation prevents age-related cognitive decline (Meck & Williams, 2003) and the decline of hippocampal proliferation in elderly rats (Glenn et al., 2008). Choline has lifelong neuronal "programming" effects that lead to enhanced hippocampal memory. How do these early-life programming effects lend themselves to non-neuronal cells, specifically neuroimmune cells? Just as prenatal immune challenges “prime” microglia toward an inflammatory phenotype in adulthood, could prenatal choline “prime” microglia against overactivation in adulthood?
In addition to this work, for two years I was the project leader of a Bass Connections team- a program focused on interdisciplinary research projects. Our team focused on Alzheimer's Disease in a mouse model, and mitigating deficits in behavior and neurobiology with voluntary exercise. This project allowed me to learn more about sex differences and aging pathology, and allowed me to develop skills in mentorship and project leadership.
Selected publications and presentations:
Maurer, S. V., Kong, C., Terrando, N., & Williams, C. L. (2019, October). Mitigating postoperative neuroinflammation with presurgical choline supplemented diet in male mice. Poster session presented at the annual meeting of the Society for Neuroscience, Chicago, IL.