Puberty is a developmental period marked by an influx of sex steroids, which trigger physical and psychological changes. Furthermore, puberty elicits changes in structural brain development that are distinct from those associated with chronological age. Emerging evidence suggests that interindividual differences in pubertal development, such as timing, whether one reaches puberty milestones before or after peers, and tempo, or whether one progresses through puberty at a slower or faster rate than peers, may also play a significant role in shaping structural brain development. The present study leverages longitudinal data from the Adolescent Brain Cognitive DevelopmentSM(ABCD Study®) to disentangle the influences of pubertal timing and tempo from chronological age on cortical and subcortical structural brain development during the adolescent period. Individuals with earlier timing tend to exhibit accelerated normative developmental trajectories compared to later timing peers, while individuals with faster tempos tend to exhibit thicker cortices, more cortical surface area, and greater subcortical volume compared to slower tempo peers. These findings underscore the significance of incorporating pubertal timing and tempo into models of structural brain development during puberty, thereby enhancing our understanding of variations in neurodevelopmental trajectories during adolescence.

Anxiety disorders are among the most prevalent mental health conditions, often emerging early in life and leading to substantial impairments across the lifespan. The bed nucleus of the stria terminalis (BNST) plays a central role in threat processing and anxiety regulation, yet its early functional connectivity profile and links to early signs of anxiety remain poorly understood. The current study investigates intrinsic functional connectivity of the BNST in 1-month-old infants using resting-state functional magnetic resonance imaging and explores its longitudinal association with anxiety symptoms later in infancy. We observe that early in development the BNST exhibits intrinsic connectivity with key subcortical regions, including the amygdala, hippocampus, and ventral striatum. However, connectivity patterns observed in human adults, including BNST–frontal cortex connectivity, were not observed in infants. Furthermore, weaker BNST–amygdala connectivity at 1 month was significantly associated with greater anxiety symptoms assessed at 18 months (β=-0.339, 95 % CI [-0.586, −0.093]), highlighting the potential role of early BNST connectivity in later anxiety-related behaviors. These findings provide the earliest evidence to date of BNST functional connectivity in human infancy and its prospective link to later anxiety symptoms, helping to fill a critical gap in our understanding of the early development of anxiety-related neural circuits.