# Psychosocial Stress and Response to Stroke

> **NIH NIH R37** · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · 2020 · $389,167

## Abstract

Project Summary
Social isolation (SI) predicts morbidity and mortality in a multitude of diseases, including cancer and
cardiovascular disease. Patients with high levels of social support or large social networks have lower risks of
developing neurodegenerative diseases such as Alzheimer's Disease (AD) and progress more slowly once
diagnosed. Whether this is also true in other amyloid related diseases such as the increasingly common
disorder of cerebral amyloid angiopathy (CAA), is not known. Social interaction overcomes the detrimental
effects of SI by promoting adaptive behaviors and favorable neuroendocrine responses to biological stressors.
We hypothesize that social interaction will reduce inflammation, enhance amyloid clearance/phagocytosis, and
increase microRNA that regulate neurotrophins such as BDNF. Despite the huge impact of SI on human
disease, no study has attempted to mitigate the detrimental effects of isolation on neurobehavioral outcomes
using target-based approaches. MicroRNAs (miRNAs) are short non-coding RNAs that are emerging as a
powerful intervention tool for many diseases including Alzheimer's Disease (AD). They regulate a broad
spectrum of biological pathways through fine-tuning of protein expression levels and altering gene expression
levels. They have the ability to concurrently target multiple effectors of pathways involved in disease pathology.
Very recent studies have found that microRNAs mediate many aspects of social interaction, leading us to
hypothesize that miRNA regulation is involved in the detrimental effects of social isolation in neurodegenerative
diseases. In this supplement we will determine which miRNAs are differentially expressed in in a mouse model
of CAA during social isolation. Both male and female mice will be used. The overall goal of this proposal is to
determine if social isolation reduces the time to symptom onset or enhances the progression of cerebral
amyloid angiopathy by effects on microRNA expression.

## Key facts

- **NIH application ID:** 10123854
- **Project number:** 3R37NS096493-05S1
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
- **Principal Investigator:** Louise D. McCullough
- **Activity code:** R37 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $389,167
- **Award type:** 3
- **Project period:** 2016-09-30 → 2023-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10123854

## Citation

> US National Institutes of Health, RePORTER application 10123854, Psychosocial Stress and Response to Stroke (3R37NS096493-05S1). Retrieved via AI Analytics 2026-05-29 from https://api.ai-analytics.org/grant/nih/10123854. Licensed CC0.

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