Funding Opportunity Number: PAR-19-385

The purpose of this funding opportunity announcement (FOA) is to stimulate research to understand the biological basis by which environmental exposures alter brain and behavioral functioning to increase risk for psychiatric disorders with onset in late-childhood, adolescence or early adulthood. The R21 grant mechanism is intended to encourage exploratory and developmental research projects that are high-risk and/or use novel approaches with potential for significant impact. Investigations that further advance our understanding of psychiatric conditions where there is less evidence of an environmental exposure link are of particular interest. A range of approaches are encouraged, from mechanistic experiments using whole organism models or in vitro and in vivo systems to human studies that add new data collection activities and/or make use of extant data or biospecimens. Investigations that further advance our understanding of the joint contribution of genes and environment in the risk for psychiatric disorders are welcomed. Applications should address either categorically defined psychiatric diagnoses and/or continuous traits expressed in the general population. Applicants are encouraged to propose studies that consider co-occurring psychiatric conditions and potential shared etiologies. It is anticipated that knowledge gained from the research supported by this FOA will inform the development of improved intervention, prevention and/or therapeutic strategies.

Application Due Dates: December 10, 2019; November 16, 2020; November 16, 2021, by 5:00 PM local time of applicant organization. All types of non-AIDS applications allowed for this funding opportunity announcement are due on these dates.

Specific Areas of Research Interest:

Topics that are appropriate for this FOA include, but are not limited to, the following:

• Alterations in level or pattern of peripheral biomarkers (e.g., cortisol, cytokines) and their role in mediating the relationship between environmental exposures and psychiatric disorders/traits
• Neural circuitry underlying toxicant-induced changes in behavioral phenotypes relevant to psychiatric disorders/traits
• Relationship(s) between environmental exposures and synaptic processes (e.g., synaptic integrity, synaptic plasticity and/or synaptic transmission) that are implicated in psychiatric disorders/traits
• Epigenetic and epigenomic alterations (e.g., histone modifications, changes in DNA methylation, non-coding RNA regulation) caused by environmental exposures and their role in mediating the association of those exposures with psychiatric disorders/traits
• Impact of environmental exposures on gut microbiome and consequences for risk of psychiatric disorders/traits
• Development and/or application of screening tools to identify and investigate, in human populations, candidate exposures that interact with biological processes implicated in psychiatric disorders/traits
• Neurobiological changes underlying how environmental chemical exposures combine with other environmental factors (e.g., microbial pathogens such as viruses, diet and nutrition, psychosocial stress, substance use, physical activity levels) to protect or increase risk for psychiatric disorders/symptoms
• Use of genetically engineered models (e.g., population-based rodent models) to identify susceptibility to exposure-related psychiatric phenotypes
• Application of functional genomics and/or novel statistical approaches to identify and validate gene-environment interactions using existing data from psychiatric studies
• Role of non-neuronal cell populations, which make up close to 90% of the cells in the brain, in the effects of environmental toxicants on psychiatric disorders/traits.