The following description is taken from the R01 version of this FOA. Participating ICs: NINR, NIMH.
Each year, millions of Americans encounter unexpected, acute illnesses. Clinical advances have resulted in increasing numbers of survivors of acute illness, yet not all survivors regain pre-illness functioning. Moreover, there is evidence that the severity of the acute insult and the presence of lingering impairments such as pain or weakness cannot account for the variability in functional recovery. One documented influence on recovery from acute illness is the occurrence of new onset depressive symptoms; specifically, depressive symptoms that are co-incident with the acute illness and which cannot be linked to the presence of a major psychological disorder. For example, incident depressive symptoms develop post-fracture in older adults and are associated with worse functional and mobility outcomes. Acute lung injury patients experience concomitant depressive symptoms that may be long lasting and impair return to optimal physical functioning. Sepsis and acute coronary syndrome are additional examples in which depressive symptoms emerge and may linger and in turn affect quality of life.
As already shown in preclinical and clinical studies, pathobiological drivers of depressive symptoms include upregulated inflammatory mediators such as cytokines. Evidence is also accumulating that immune challenges can unfavorably shift the gut microbiome to one that promotes an inflammatory milieu and adversely affect the brain and hence behavior. Other potential influences include oxidative stress, epigenetic changes and altered neural circuits. Considering that depressive symptoms are a risk factor for optimal recovery, a better understanding of the etiology of depressive symptoms in the context of acute illness and return to pre-illness functioning is needed. This concept proposes to address this gap by encouraging research on new onset depressive symptoms. A key aspect of this concept is use of a common framework for the proposed research: observational studies of carefully-phenotyped individuals to assess pathobiological biomarkers in the early stages of the acute illness and during the recovery trajectory, in conjunction with ongoing measures of depressive symptoms.
In summary, increasing numbers of patients survive acute illness yet their return to pre-illness functioning is not guaranteed; new onset depressive symptoms are a contributing factor to suboptimal recovery. An improved understanding of the etiology of new onset depressive symptoms has the potential to minimize the long-term sequelae of acute illness. Identifying the pathobiological underpinnings of incident depressive symptoms may inform clinical interventions and prevent depressive symptoms from becoming an independent condition requiring pharmacologic therapies.
Research Objectives include, but are not limited to, those that address:
- Investigate biomarkers including those related to inflammation and oxidative stress as pathobiological drivers of new onset depressive symptoms in acute illness
- Characterize trajectories of pathobiological markers during the acute and post-acute illness and recovery phases in individuals experiencing new onset depressive symptoms
- Utilize omics technologies to identify mechanistic pathways that underpin new onset depressive symptoms
- Test the relationship between biomarkers of depressive symptoms and return to pre-illness functioning following the onset of acute illness
- Assess bidirectional links between inflammation and depressive symptoms in relation to sex/gender
This FOA is intended to encourage preclinical and clinical research such as observational trials. Clinical trials are not allowed for this FOA. Clinical research that focuses on individuals with major depressive disorder or clinically diagnosed depression is not appropriate for this FOA. Potential applicants are encouraged to contact the NINR Scientific/Research Contact to discuss proposed research ideas prior to submission of the application.
Interdisciplinary collaborations that include nurse scientists in the project team are strongly encouraged.
Deadlines: standard dates (and AIDS dates) apply
- R01 – https://grants.nih.gov/grants/guide/pa-files/PA-17-488.html
- R21 – https://grants.nih.gov/grants/guide/pa-files/PA-17-487.html
Filed Under: Funding Opportunities