# From Social Discruption to Neural Compromise: Establishing Markers and Mediators

> **NIH NIH R01** · OHIO STATE UNIVERSITY · 2024 · $82,309

## Abstract

Humans are generally social and these social relationships can promote a healthier lifestyle and
increase longevity. Yet, when these social relationships are lost or come to an end, the perceived
social isolation and accompanying loneliness can lead to significant physiological, psychological,
and social consequences that impair an individual’s ability to function and greatly impairs their
quality of life. Although it is widely recognized that social bonds contribute to health, the
mechanism(s) by which social bond disruption translates into compromised mental and physical
health are not fully appreciated. An understanding of the biological substrates that drive social
bonds, and the negative sequelae following loss of social bonds, is essential to develop a
framework for pharmacological interventions to reduce health risks associated with loneliness.
The conditions and disorders associated with loneliness have each been linked to inflammation
and metabolic disruption. The proposed studies will determine the extent to which social bond
disruption engages inflammatory and metabolic substrates in the brain of a social species. Given
that the negative effects of loneliness are not simply ameliorated by the presence of other
individuals in humans, it is essential to examine the underlying protective mechanisms of social
bonds, and the biology engaged when bonds are broken, in order to develop interventions aimed
at optimizing physical and psychological outcomes for those lacking positive social support. The
overarching hypothesis of this line of inquiry is that the neural-glial response engaged by social
bond disruption increases neuroinflammation and compromises neural mitochondrial function
through disruptions in oxytocin (OT) signaling. Using the socially and genetically monogamous
California mouse (Peromyscus californicus), we will determine the extent to which pair bond
dissolution increases the neuroinflammatory response to challenge and the extent to which
stress-related behaviors can predict the anticipated inflammatory response to pair bond
dissolution (Aim 1). We will also test whether pair bond dissolution disrupts synaptosome
mitochondrial function (Aim 2). Lastly, we will determine to what extent OT can ameliorate the
impact of pair bond dissolution on the neural-glial axis (Aim 3). The impact of social experiences
on the brain may be critical to understanding the biological drivers of mental health disorders and
neurodegenerative conditions, like Alzheimer’s Disease and related dementias.

## Key facts

- **NIH application ID:** 10984301
- **Project number:** 3R01NS125589-03S1
- **Recipient organization:** OHIO STATE UNIVERSITY
- **Principal Investigator:** Erica R Glasper
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $82,309
- **Award type:** 3
- **Project period:** 2021-12-01 → 2026-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10984301

## Citation

> US National Institutes of Health, RePORTER application 10984301, From Social Discruption to Neural Compromise: Establishing Markers and Mediators (3R01NS125589-03S1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10984301. Licensed CC0.

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