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The Rouzer IDEAL Lab studies how developmental substance exposures influence brain and behavioral health across the lifespan. By integrating controlled preclinical models with evidence from existing human datasets, we identify findings that converge across approaches and use them to refine our research questions and models.
Principles Guiding Our Research
We approach developmental substance exposure without stigma, judgment, or blame.
We incorporate sex as a biological variable throughout study design, analysis, and interpretation, allowing us to identify both shared and sex-dependent patterns of vulnerability and resilience.
We approach our experiments with the intention of generating knowledge that advances understanding, informs clinical and public health practice, and better supports affected individuals and families.
Alcohol and cannabinoids are often studied as separate prenatal exposures, even though they are commonly used together, and combined exposure may influence development differently from either substance alone (Rouzer et al., 2023). The Rouzer IDEAL Lab uses developmentally timed mouse models to compare prenatal alcohol exposure, cannabinoid exposure, and their co-exposure.
Through this work, we aim to determine which outcomes are specific to co-exposure, whether effects differ by sex or developmental stage, and how changes in brain systems involved in decision-making and motivated behavior relate to long-term outcomes. By identifying effects that may be missed when alcohol and cannabinoids are studied separately, we can develop more representative models of prenatal polysubstance exposure and generate evidence that can guide future clinical research, support, and intervention.
Research examining how parental alcohol use around conception affects offspring development has historically focused on maternal alcohol exposure, leaving paternal and dual-parent contributions comparatively understudied. However, we know that in humans, each partner’s drinking habits can influence the other partner’s drinking over time, making shared drinking patterns and dual-parent alcohol exposure a relevant real-world scenario (Bartel et al., 2017). We use a model that directly compares control, maternal, paternal, and dual-parent alcohol exposures to determine whether each parental source produces shared, distinct, or interacting effects in offspring.
By comparing these exposure histories within the same experiments, we aim to develop a more complete understanding of how alcohol exposure in either or both parents can shape long-term brain and behavioral health and to identify outcomes that may require distinct forms of assessment or support. Prior work with this model has identified both overlapping and exposure-specific effects on adolescent behavior (Thomas et al., 2025).
Findings from controlled models are most useful when they can be evaluated alongside patterns observed in people. We use existing human datasets to ask whether behavioral and biological outcomes identified in our preclinical studies are also associated with comparable developmental exposure histories in human populations. By looking for convergence across behavior, gene activity, protein expression, and brain function, we can identify findings with the greatest translational relevance while also recognizing where the complexity of human experiences is not fully captured by current models. This work will help us refine our experimental models, identify outcomes that may warrant closer assessment or additional support, and prioritize targets for future prevention and intervention research.
We use carefully controlled mouse models to determine how exposure combinations, exposure timing, and maternal, paternal, or dual-parent exposures influence development. We follow offspring through adulthood and integrate behavioral testing with molecular and proteomic analyses, transcriptomics, and electrophysiology to connect long-term outcomes with changes in brain cells, synapses, and circuits. Across these studies, we examine both shared and sex-dependent responses to developmental exposures.
We conduct secondary analyses of existing human datasets containing information about developmental exposures, substance use, behavior, health, and biological variation. Depending on the available data, we use multivariable and longitudinal models to examine exposure–outcome relationships, conduct sex-stratified analyses, and analyze genomic or transcriptomic data to identify associated genes, gene networks, and biological pathways. We then compare these patterns with behavioral, molecular, and neural findings from our preclinical studies, focusing on convergence across related outcomes and pathways rather than requiring identical measurements across species.