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Influence of social environment on the neural mechanisms of sickness

Award Number: F32MH140490
ORGANIZATION: NATIONAL INSTITUTE OF MENTAL HEALTH
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 06/01/2026
PERIOD OF PERFORMANCE END DATE: 05/31/2029

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Influence of social environment on the neural mechanisms of sickness - PROJECT SUMMARY During sickness, the immune system and central nervous system coordinate to generate physical and behavioral changes, such as lethargy, anorexia, anhedonia, and social withdrawal, that can vary significantly in severity between individuals. While these symptoms help aid in sickness recovery, severe responses can be harmful and possibly life-threatening. What drives this symptomatic variation in sickness manifestation is still unclear, however, external factors such as social support may be a contributing factor. Prolonged social isolation not only impacts the immune response but is also associated with adverse physical and mental health outcomes. Previous studies have identified bi-directional interactions between immune signals and the central nervous system, suggesting a direct link between immune-activated neural circuits and sickness outcomes. Moreover, social isolation can have a dramatic effect on neuronal activity in specific brain regions. My preliminary studies demonstrate that social isolation exacerbates symptoms of sickness, such as body temperature and appetite, and increases circulating levels of immune factors known to mediate sickness state. Using activity pattern analysis, I found that activity in the insular cortex (IC) is dependent on both sickness and social isolation, suggesting integration of both social and immune signals. Therefore, I hypothesized that social isolation increases the severity and recovery time of sickness through specific neuronal and circuit mechanisms that integrate social behavior and sickness. I will address my central hypothesis by inducing sickness in isolated or group-housed mice through peripheral administration of bacterial lipopolysaccharides (LPS). In Aim 1, I will employ cell-type-specific functional manipulation approaches, including chemogenetic activation and permanent neuronal silencing, to determine the function of the “sickness neurons” in the IC. In Aim 2, I will identify the upstream neuronal inputs that convey social context to sickness-activated IC neurons using retrograde tracing and determine how these social inputs modulate sickness symptoms and behaviors using projection-specific activation. Together, the completion of this project will determine how the social environment influences sickness manifestation and recovery, revealing critical insight into long-standing observations linking isolated social environments with poor health.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $79,348 )
2026	2026	UNIVERSITY OF UTAH	201 PRESIDENTS CIR	SALT LAKE CITY	UT	84112	SALT LAKE	USA	Mental Health Research Grants	001	1	5/7/2026	NEW	$0
2026	2026	UNIVERSITY OF UTAH	201 PRESIDENTS CIR	SALT LAKE CITY	UT	84112	SALT LAKE	USA	Mental Health Research Grants	000	1	5/7/2026	NEW	$79,348
														Subtotal = $79,348

Grand Total All Awards = $79,348

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Influence of social environment on the neural mechanisms of sickness

Award Number: F32MH140490

ORGANIZATION: NATIONAL INSTITUTE OF MENTAL HEALTH

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 06/01/2026

PERIOD OF PERFORMANCE END DATE: 05/31/2029

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