# AD Supplement to Hypoth neuron activation to blunt myocar remodeling during chronic sleep apnea

> **NIH NIH R01** · GEORGE WASHINGTON UNIVERSITY · 2020 · $398,750

## Abstract

PROJECT SUMMARY
Our previous work and the ongoing studies of our parent grant reveal that a novel intervention, chronic activation
of hypothalamic oxytocin neurons, prevents the hypertension that develops with chronic exposure to intermittent
hypoxia (CIH), an animal model of obstructive sleep apnea (OSA). This treatment paradigm also restores
autonomic balance, significantly reduces inflammation, and improves cardiovascular health. Our animal studies
have provided a foundation for our clinical studies in which we have found that a single intranasal dose of
oxytocin in patients with OSA increased their total sleep time and self-reported sleep satisfaction. Our analysis
of the 8-hour polysomnography data from those studies further indicates that intranasal oxytocin reduced both
the duration and oxygen desaturations of hypoxic events. These results altogether demonstrate that our novel
target of activating the oxytocin network within the hypothalamus can be beneficial in reducing both the severity
and deleterious widespread consequences of OSA, and that our animal work (currently supported by
R01HL146169) and our treatment paradigm has high translational potential. This Administrative Supplement will
examine our central hypothesis that both hypothalamic oxytocin neuron activation and intranasal oxytocin, in
addition to reducing the development of hypertension during CIH, will reduce autonomic dysfunction and CNS
inflammation, thereby mitigating the initiation and progression of cognitive decline and Alzheimer disease
markers that occur with OSA. We will leverage new advances in the parent grant, such as hypothalamic oxytocin
neuron activation and intranasal oxytocin as novel treatment targets. In this supplement, we will test, in the same
groups of animals required to complete the goals in the parent grant, whether or not hypothalamic oxytocin
neuron activation and intranasal oxytocin reduces amyloid beta deposition, neurofibrillary tangles, neuronal
apoptosis, and cognitive decline that occurs in animals chronically exposed to CIH. We will use several core
facilities, including the GW Behavioral Core for assessments of cognitive function and the GWU Imaging Core
for quantification of amyloid beta deposition, neurofibrillary tangles and neuronal apoptosis to test our hypothesis.
Our supplement has one overarching Specific Aim: To test the hypothesis that chronic hypothalamic oxytocin
neuron activation and daily intranasal oxytocin administration will both independently reduce the amyloid beta
deposition, neurofibrillary tangles, neuronal apoptosis, and cognitive decline that occurs with CIH.

## Key facts

- **NIH application ID:** 10123619
- **Project number:** 3R01HL146169-02S1
- **Recipient organization:** GEORGE WASHINGTON UNIVERSITY
- **Principal Investigator:** Matthew W. Kay
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $398,750
- **Award type:** 3
- **Project period:** 2018-12-21 → 2022-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10123619

## Citation

> US National Institutes of Health, RePORTER application 10123619, AD Supplement to Hypoth neuron activation to blunt myocar remodeling during chronic sleep apnea (3R01HL146169-02S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10123619. Licensed CC0.

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