Social relationships are critical for human health and happiness. These relationships are so important that we enter the world seemingly primed to take in social information; within the first few hours of life, newborns already show a perceptual bias to social stimuli like faces and voices. These early perceptual biases are thought to set the stage for subsequent social-cognitive abilities – such as the ability to understand the thoughts and emotions of others – that ultimately facilitate the formation of critical social relationships. However, the degree to which different individuals show these perceptual biases and are ultimately successful at advanced social-cognitive processes varies, and some cases may be indicative of disorders like autism.

Our research aims to identify and characterize the neurobiological and neurodevelopmental factors that contribute to individual differences in social abilities. Taking an environmennt-gene-brain-behavior, lifespan development, individual differences approach, we employ techniques including genetic, epigenetic and hormonal assays; EEG and fMRI; eye-tracking, self-report questionnaires, videotaped real-world social interactions, and performance on social-cognitive tasks; and computational modeling to understand, predict, and improve social outcomes for all individuals.



The first year of life constitutes a time of rapid and sweeping changes in behavioral repertoire, cognitive ability, and neural architecture. During this time, developing infants are confronted with the daunting task of making sense of the world as they are bombarded with competing, fluctuating, and often ambiguous external stimuli. Understanding how the brain comes to form accurate models of the external world and generate appropriate behavioral responses is a significant and critical question of widespread multidisciplinary interest. Social information represents a particularly important and complex class of stimuli that evoke unique neural and behavioral responses beginning in infancy. However, some infants go on to struggle in a social environment, while others navigate the complex social world with ease.

Current research questions include:

  • Can we identify predictive biomarkers for social difficulties that emerge before behavioral symptoms?

  • Are there particular patterns of gene or brain activity, or “biotypes,” that can parse the highly heterogenous and complex social behavioral phenotype?

  • How can we intervene to optimize social neurodevelopmental outcomes for all children?


Variability is a fundamental property of neural systems at multiple hierarchical levels, from the dynamics of ion channels to the convergence of multiple independent synaptic inputs. Such moment-to-moment temperodynamic variability in neural signal, which is often modeled out of analyses as mere “noise,” is increasingly understood to serve a valuable functional role. For example, a moderate amount of random noise in a signal can counterintuitively enhance signal detection by improving the fidelity of an underlying signal. In the context of brain signaling, temperodynamic variability can facilitate the exchange of information between neurons, enhance neural synchrony, and promote the formation of robust, adaptable networks that are not overly reliant on any particular node and display a greater dynamic range. Together, these functions suggest that temperodynamic neural variability may act to appropriately weight incoming information such that important stimuli are maximally salient and enable the most flexible behavioral response.

Current research questions include:

  • What neurobiological factors drive individual differences in temperodynamic neural variability?

  • Under what contexts can temperodynamic neural variability be exploited to impact behavior?

  • How do onset and quantity of temperodynamic neural variability interact to impact neurodevelopmental outcomes? (Too little too late? Too much too soon?)


We seek to understand what molecular and neurobiological factors impact social behavior across the lifespan. For example, oxytocin is a peripheral hormone and central neuromodulator with particular relevance for social behavior. The actions of oxytocin are dependent upon its receptor, which undergoes an epigenetic modification called DNA methylation. Unlike genetic changes which are often “all or none,” epigenetics can be thought of as a “dimmer switch” on gene expression. People with more DNA methylation along certain regions of their oxytocin receptor gene (OXTR) have reduced gene expression, and therefore presumably decreased ability to use the oxytocin in their body. While popularized as a “love” hormone, oxytocin actually has broad effects across the body, and sometimes seemingly contradictory effects on social behavior.

Current research questions include:

  • How does oxytocin impact basic biological systems to regulate social behavior, such as those that facilitate the detection of and orientation to social information?

  • How do interactions among and between molecular systems regulate brain activity during social tasks?

  • Are there periods of plasticity during which the molecular systems that support social functions are particularly malleable?