Research

How is memory and its underlying neurobiology affected across the lifespan?

One question runs through everything below: why does memory hold up with age for some people and not others, and how much of that difference is written by the environments people live in? The hippocampus and the wider medial temporal lobe are not fixed at birth. They are built, maintained, and eroded continuously, and the conditions a person encounters along the way leave marks on those systems: air pollution, neighborhood resources and opportunity, room for physical activity, chronic stress.

My work asks where and when those exposures matter, which neural features carry the effect, and what makes some people resilient to them. Because the answer almost certainly differs by life stage, I work across the lifespan rather than within a single age band: neurodevelopment in childhood and adolescence, fitness and psychosocial stress in adulthood, and neighborhood context and cognitive aging in older adults.

Environmental Exposures and the Developing Brain

My current research focuses on the impact of ambient fine particulate matter (PM_2.5) air pollution on neurodevelopment, particularly how these exposures influence the structure and function of memory-related brain systems. I apply expertise in structural neuroimaging to investigate how pollutant mixtures affect hippocampal microstructure and long-axis segmentation. In work published in BMC Medicine (2026), I found that specific components and sources of ambient pollution—not simply total mass—were associated with hippocampal architecture and memory performance in pre-adolescents. That distinction matters because air quality standards are largely written around total mass. In the Herting lab, I’ve also contributed to a scoping review on air pollution’s impact on neurodevelopment and an empirical study assessing how air pollution sources relate to cortical structure in pre-adolescents.

Co-Exposures and Emerging Psychopathology

Air pollution and early life adversity are two faces of the same question: what is a child’s environment actually made of? They are usually studied separately, which leaves open whether they bear on mental health together. With Amanda Del Giacco, as co-first authors, I asked whether the two are jointly related to psychopathology symptoms and to the amygdala subregions implicated in them. Ambient PM_2.5 moderated the association between early life adversity and specific externalizing symptoms: children facing both higher adversity and higher pollution showed the greatest symptoms. The amygdala tracked adversity as well—among youth with higher early life adversity, smaller volumes in the basolateral paralaminar subregion—a part of the amygdala involved in emotional learning and threat processing—were linked to greater general and specific externalizing symptoms. Neither exposure told the whole story on its own, which is the practical upshot—identifying children at risk means reading the psychosocial and physical environment together rather than one at a time. This work is available as a preprint: bioRxiv, 2026.

Environmental Enrichment and Memory Performance

In parallel, I study how enriched neighborhood environments shape memory development. Working with Dr. Wesley Thompson, I examined how brain structure and function carry the association between environmental enrichment (indexed via the Childhood Opportunity Index 2.0) and episodic memory in 9- to 13-year-olds. The route turned out to be prefrontal rather than medial temporal: working memory activity in prefrontal cortex partially mediated the link between enrichment and episodic memory, while medial temporal pathways did not account for it. That points attention toward the executive scaffolding around memory rather than the memory structures themselves. This work is published in Brain and Environment (2026).

Fitness and Medial Temporal Lobe Structure

During my PhD, I investigated the role of cardiorespiratory fitness in modulating brain structure across the medial temporal lobe. Using surface-based neuroimaging methods, I found that higher fitness levels in young adults were associated with increased cortical thickness in the entorhinal, parahippocampal, and perirhinal cortices—regions critical to spatial cognition and memory. This association was not observed in older adults, suggesting age-specific sensitivity to fitness-related neuroplasticity. This work resulted in a first-author publication: EJN, 2024.

Psychosocial Stress and Hippocampal Structure in Older Adults

Also during my PhD, I examined how chronic psychosocial stress, particularly perceived discrimination, relates to medial temporal lobe structure among older adults. I found that greater perceived discrimination was associated with smaller anterior hippocampal and amygdala volumes—brain regions involved in memory and emotion regulation. Importantly, higher levels of personal mastery (i.e., perceived control and agency) appeared to buffer these effects. Among individuals with high mastery, the relationship between discrimination and brain volume was no longer significant. This work is available as a preprint: bioRxiv, 2024.