In March 2020, New York City was the epicentre of the COVID-19 epidemic in the US. COVID-19 has the potential to have a profound impact on pregnant women and their offspring because pregnant women are particularly susceptible to respiratory pathogens as they are in a state of immune tolerance and relatively intolerant to hypoxia. The very limited data on the effects of SARS-CoV-2 during pregnancy suggest a relation between COVID-19 and an increased risk for emergency C-sections, preterm birth and neonatal distress. Data from previous coronavirus epidemics (SARS and MERS) suggest associations with severe maternal illness, maternal death, and severe adverse child outcomes. Further, the COVID-19 pandemic may exacerbate current inequalities in maternal and infant health. While emerging data has demonstrated that communities of color are being impacted most by this pandemic, little data is available on the impact of SARS-CoV-2 on pregnant women of color and their offspring. The effects of COVID-19 on maternal mortality and morbidity, birth outcomes, and health disparities require urgent investigation.

Consequently, we are conducting a prospective pregnancy cohort study with thorough assessments of SARS-CoV-2 infection and immune response in all pregnant women (symptomatic and asymptomatic), and in-depth assessment of electronic medical records to establish pregnancy, fetal, and neonatal outcomes.

The number of refugees around the world who are fleeing violence or persecution in their home countries in search of safety abroad has grown dramatically over the past decade. At the end of 2016, a record number of 65.6 million people around the world were forcibly displaced (United Nations High Commissioner for Refugees, Figures at a glance 2017). The United States has long been a global leader in the resettlement of refugees, with approximately 3 million individuals resettling in the USA since 1975 (approximately 2 million adults and 1 million children) (Office of Refugee Resettlement, Fiscal year 2012 refugee arrivals) in the hope of a better life.

Many refugees fleeing their homes are ill-equipped with the financial, linguistic, and other resources needed to address the challenges of the journey ahead, which is frequently marked by fear, violence, and trauma. As a result, many refugees resettling in third-party countries often experience mental health problems associated with past trauma, the ongoing stress of resettlement, or both. As the numbers of forcibly displaced people continues to rise, understanding the immediate and long-term impacts of the refugee experience and cultural context on psychological functioning become essential.

We are studying the effects of traumatic experiences, daily stressors of resettlement, and resilience on the mental health of migrants arriving at the Southern border, and plan to repeat the assessments six and 12 months later. Insight gained from this information will aid in effectively serving this population by informing policy makers and clinicians.

Brain structural abnormalities have been consistently documented in childhood developmental disorders, including autism and ADHD. However, the developmental origins of these brain abnormalities remain largely unknown. Several lines of evidence point to the perinatal period as potentially important since fetal development is a sensitive time window for brain growth and neurodevelopment. A number of studies have found significant negative associations between levels of phthalate metabolites in prenatal urine and child cognitive functions, behavioral outcomes, mental and psychomotor development, and neonatal and infant neurological status. In addition, a dose-response relationship between prenatal acetaminophen exposure and risk of adverse neurodevelopmental outcomes has been reported. However, these studies have relied on recalled exposure and did not investigate fetal brain development. In this pilot, we are investigating how early prenatal exposure to phthalates, acetaminophen and antidepressants affect fetal brain volume, as well as child development and health.

Understanding mechanisms underlying comorbid disorders poses a challenge for developing precision medicine tools. Psychiatric disorders are highly comorbid, and are among the last areas of medicine, where classification is driven by phenomenology rather than pathophysiology. The CoCA project investigates comorbidity between the most frequent psychiatric conditions: ADHD, mood/anxiety, and substance use disorders, and a highly prevalent somatic disease, namely obesity.

ADHD, a childhood-onset disorder, forms the entry into a lifelong negative trajectory characterized by these comorbidities. Common mechanisms underlying this course are unknown, despite their relevance for early detection, prevention, and treatment. Our interdisciplinary team of experts integrates epidemiologic/genetic approaches with experimental designs to address those issues. We are determining disease burden of comorbidity, calculate its socioeconomic impact, and reveal risk factors. We are studying biological pathways of comorbidity and derive biomarkers, prioritizing two candidate mechanisms (circadian rhythm and dopaminergic neurotransmission), but also leveraging large existing data sets to identify new ones.

I are conducting a randomized, single-blinded, controlled pilot study to establish effect sizes of exercise and bright light therapy in combination with mHealth based reinforcement on general health, obesity, ADHD and depressive symptoms in adolescents and young adults with ADHD. These non-pharmacological treatments are known to modulate dopamine and the circadian rhythm, respectively. The CoCA project aims to facilitate early detection of ADHD, as well as non-invasive, scalable, and low-cost treatment, creating opportunities for substantial and immediate societal impact.

Children and adolescents born preterm are at a significantly increased risk for developing attention deficit hyperactivity disorder (ADHD) and are reported to have similar impairments in cognitive and regulatory processes; yet the underlying risk pathways remain poorly understood. In this study, we identified cognitive and neurophysiological impairments that sensitively index the genetic risk for ADHD, and specified their inter-relationships. In SPIN we assessed 150 preterm-born adolescents and their siblings on our detailed cognitive-electrophysiological test battery, and directly compared these data to data already collected from ADHD and control sibling pairs. This allowed us to evaluate whether the same impairments linked to genetic risk for ADHD are also seen in preterm children. In familial risk analyses we will further investigate whether, in the preterm-born group, the same underlying impairments have an environmental etiology. By investigating biomarkers for the underlying processes linked to the increased risk for ADHD among children born preterm, we aim to identify cognitive dysfunctions that can be targeted for early identification and intervention. We further investigated whether the cognitive-neurophysiological impairments in the preterm-born group are linked specifically to ADHD symptoms or also to other psychiatric symptoms, such as anxiety, social difficulties and autism spectrum symptoms.