Adolescent development is not only shaped by the mere passing of time and accumulating experience, but it also depends on pubertal timing and the cascade of maturational processes orchestrated by gonadal hormones. Although individual variability in puberty onset confounds adolescent studies, it has not been efficiently controlled for. Here we introduce ultrasonic bone age assessment to estimate biological maturity and disentangle the independent effects of chronological and biological age on adolescent cognitive abilities, emotional development, and brain maturation. Comparing cognitive performance of participants with different skeletal maturity we uncover the impact of biological age on both IQ and specific abilities. With respect to emotional development, we find narrow windows of highest vulnerability determined by biological age. In terms of neural development, we focus on the relevance of neural states unrelated to sensory stimulation, such as cortical activity during sleep and resting states, and we uncover a novel anterior-to-posterior pattern of human brain maturation. Based on our findings, bone age is a promising biomarker of adolescent maturity.

Research evidence indicates that psychosocial stressors such as work-life stress serves as a negative occupational exposure relating to poor health behaviors including smoking, poor food choices, low levels of exercise, and even decreased sleep time, as well as a number of chronic health outcomes. The association between work-life stress and adverse health behaviors and chronic health suggests that Occupational Health Psychology (OHP) interventions such as leadership support trainings may be helpful in mitigating effects of work-life stress and improving health, consistent with the Total Worker Health approach. This presentation will review workplace psychosocial stressors and leadership training approaches to reduces stress and improve health, highlighting a randomized controlled trial, the Military Employee Sleep and Health study.

The human brain is a heavily interconnected structure giving rise to complex functions. While brain functionality is mostly revealed during wakefulness, the sleeping brain might offer another view into physiological and pathological brain connectivity. Furthermore, there is a large body of evidence supporting that sleep mediates plastic changes in brain connectivity. Although brain plasticity depends on environmental input which is provided in the waking state, disconnection during sleep might be necessary for integrating new into existing information and at the same time restoring brain efficiency. In this talk, I will present structural, molecular, and electrophysiological markers of brain connectivity and sleep-dependent restoration that we have evaluated using Magnetic Resonance Imaging and electroencephalography in a healthy population. In a second step, I will show how we translated the gained findings into two clinical populations in which alterations in brain connectivity have been described, the neuropsychiatric disorder attention-deficit/hyperactivity disorder (ADHD) and the neurologic disorder thalamic ischemic stroke.