# Inflammatory contributions of astrocytic RelA in comorbid VCID/AD

> **NIH NIH RF1** · UNIVERSITY OF KENTUCKY · 2021 · $354,501

## Abstract

PROJECT SUMMARY/ABSTRACT
Multiple lines of evidence in both humans and animal models suggest that neuroinflammation, mediated via
reactive gliosis, plays a critical role associated with the initiation and progression of vascular contributions to
cognitive impairment and dementia (VCID) and Alzheimer’s disease (AD), potentially suggesting convergent
pathophysiological mechanisms. In particular, several of these neuroinflammatory hallmarks in comorbid
VCID/AD animal models have been linked with the dysfunctional responses of reactive astrocytes. In the
healthy brain, it is well known that astrocytes play a critical role in maintaining a variety of homeostatic
mechanisms. However, as a response to injury or disease, astrocytes are able to rapidly respond, in a
generalized description referred as astrogliosis, with a variety of neuroinflammatory modalities, which recent
evidence suggests may cause dysfunctional responses of neurons. Sleep disturbances/circadian disruption is
a key clinical issue in dementia patients. Between 40 and 70% of older adults suffer from sleep disturbances or
disorders, which are especially prevalent among patients with Alzheimer's Disease and Alzheimer’s Disease
Related Dementias (AD/ADRD), such as VCID. The purpose of this one-year administrative supplement is to
facilitate new collaborative research between the Morganti and Duncan labs to better understand the bi-
directional relationship between chronic sleep disturbances/circadian disruption and VCID pathogenesis in the
context of inflammatory mechanisms of astrocytes. This proposal will examine 2 focused specific aims, which
are extensions of our ongoing projects in the parent grant RF1NS118558:
 1. Determine the extent to which chronic sleep fragmentation drives astrocyte-specific inflammatory
 heterogeneity in the context of VCID, and whether removal astrocytic-RelA disrupts these transcriptional
 and morphological phenotypes.
 2. Determine the extent to which chronic sleep fragmentation alters cognitive function, and whether
 removal astrocytic-RelA disrupts these phenotypes.

## Key facts

- **NIH application ID:** 10401633
- **Project number:** 3RF1NS118558-01S1
- **Recipient organization:** UNIVERSITY OF KENTUCKY
- **Principal Investigator:** Josh Morganti
- **Activity code:** RF1 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $354,501
- **Award type:** 3
- **Project period:** 2021-09-01 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10401633

## Citation

> US National Institutes of Health, RePORTER application 10401633, Inflammatory contributions of astrocytic RelA in comorbid VCID/AD (3RF1NS118558-01S1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10401633. Licensed CC0.

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