Our Research:

The prenatal environment contains a complex mixture of metabolic, inflammatory, and environmental signals. These signals are interpreted by both the placenta and the developing nervous system, shaping developmental trajectories in ways we are only beginning to understand. The Campbell Lab investigates how these early biological interactions influence neural development and contribute to autism and other developmental disorders.

Our work spans the maternal–fetal interface to the developing brain. We combine stem-cell and organoid systems, animal models, engineered human-relevant platforms, molecular biology, and advanced imaging. Across these approaches, we are especially interested in redox biology: how cells sense, use, and respond to changes in their oxidative environment during development.

Next-generation tools for studying redox biology

Redox signaling is essential to normal cell function, but its dynamics during brain development remain poorly understood. Developing cells must regulate their redox state while undergoing proliferation, differentiation, migration, and maturation. Disruption of this balance may create periods of heightened vulnerability to environmental, inflammatory, or metabolic stress.

We develop and apply next-generation genetically encoded sensors to observe redox biology in living developmental systems. These tools allow us to investigate when redox states change, how different cells respond to stress, and whether recovery trajectories can reveal mechanisms of resilience or vulnerability. By making redox biology visible across time and space, we aim to uncover fundamental principles of normal development and identify pathways relevant to developmental disorders.

Environmental exposures and developmental vulnerability

Environmental exposures during pregnancy—including pollutants, pesticides, industrial chemicals, medications, and other commonly encountered compounds—may influence fetal development in ways that are difficult to predict from maternal dose alone. The timing of an exposure, the developmental state of the affected cells, and the capacity of the placenta and fetus to respond to oxidative stress may all shape its biological consequences. We seek to identify critical windows of susceptibility and understand why particular developmental processes or cell populations are especially vulnerable.

Using complementary animal, stem-cell, organoid, and engineered human-relevant models, we investigate how prenatal exposures alter redox signaling, cellular metabolism, placental function, and early neural development. Rather than treating oxidative stress only as a marker of toxicity, we study its dynamics—including the magnitude, timing, and recovery of the response—to distinguish transient adaptation from persistent disruption. This work aims to provide a mechanistic foundation for developmental neurotoxicology and ultimately improve how environmental risks to the developing brain are identified and evaluated.

The placental barrier and the developing brain

The placenta is not simply a passive barrier between mother and fetus. It regulates the transfer of molecules, responds to environmental conditions, and produces signals that can influence fetal development. Yet many experimental models of neurodevelopmental exposures largely omit the placenta, making it difficult to determine what the developing brain actually encounters.

We are building human-relevant experimental systems that connect models of the placental barrier with models of early neural development. These platforms allow us to study how placental transport, stress responses, and signaling shape downstream developmental effects without assuming that maternal and fetal exposures are equivalent. This work seeks to establish the placenta as a central component of developmental neuroscience and improve how prenatal risks are investigated.

Viral infection, placental function, and neurodevelopment

Viral infections during pregnancy have been associated with adverse pregnancy and developmental outcomes, but the biological pathways connecting maternal infection with fetal brain development remain incompletely understood. The placenta may be a particularly important part of this connection because infection can affect its barrier function, inflammatory signaling, oxidative state, and capacity to support fetal development.

Using human placental tissue and engineered models of the maternal–fetal interface, we study how viral exposures alter placental biology and whether those changes influence early neuronal development. Our goal is to understand when the placenta protects the developing fetus, when its function becomes disrupted, and which placental responses may provide insight into later developmental risk.

Modeling autism heterogeneity with cortical organoids

Autism encompasses substantial biological and clinical heterogeneity, yet many experimental studies treat it as a single condition. This can obscure developmental mechanisms that may differ across individuals and contribute to distinct developmental trajectories.

In collaboration with colleagues at UC San Diego, we use participant-derived cortical organoids to study early features of brain development associated with autism. We examine developmental processes such as growth, neural progenitor behavior, differentiation, migration, and metabolism, and relate cellular findings to deeply characterized clinical profiles. By connecting early developmental biology with individual differences, this work aims to provide a more precise understanding of autism and its diverse forms.

Signaling and neural cell identity

The cerebral cortex depends on a diverse population of inhibitory interneurons to regulate neural circuits. Disruption of interneuron development has been implicated in autism, epilepsy, schizophrenia, and other neurological and psychiatric conditions. However, the mechanisms that generate distinct interneuron identities during development remain unresolved.

We study how extracellular signals are interpreted by developing neural cells to guide cell fate. A major focus is Ryk, a non-canonical Wnt receptor that influences the development of cortical interneuron populations. By investigating how Ryk interacts with other developmental pathways and with the regulatory state of the cell, we seek to understand how transient signals produce lasting differences in neural identity and circuit function.

A connected view of prenatal development 

Together, these projects address a shared question: how do signals encountered during prenatal development become lasting biological outcomes? By studying redox regulation, placental function, developmental exposures, human neural models, and cell-fate signaling together, we hope to build a more integrated understanding of developmental vulnerability and resilience.

Our interdisciplinary research creates opportunities for scientists from neuroscience, placental biology, developmental biology, stem-cell biology, bioengineering, metabolism, toxicology, virology, and quantitative imaging. We welcome researchers who want to build new experimental systems and use them to answer consequential questions about early human development.