# Neurocognitive Consequences of Intermittent Hypoxia

> **NIH NIH R01** · UNIVERSITY OF CHICAGO · 2020 · $405,000

## Abstract

Abstract
Alzheimer's disease (AD) is a debilitating neurodegenerative disease responsible for cognitive impairment and
dementia. An estimated 13 million Americans will suffer from AD by the year 2050. Approximately half of these
individuals will suffer from sleep apnea. While sleep apnea is known to independently cause cognitive deficits,
it also worsens AD. Sleep apnea facilitates early onset of AD and exacerbates AD associated dementia.
Additionally, when sleep apnea is treated in AD patients, cognition is significantly improved. Despite evidence
of strong links between sleep apnea and AD, there is a limited understanding into the mechanistic
entanglement of these two conditions. This gap in knowledge likely contributes to the lack of effective
therapies for AD and AD associated dementias. Our research addresses this issue by examining how
intermittent hypoxia (IH), a primary consequence of sleep apnea, adversely effects AD neuropathology in an
AD mouse model. Our work indicates that IH stimulates activity from the carotid bodies to increase
hippocampal oxidative stress, which may worsen AD pathology. These new observations suggest that carotid
bodies, the primary organs responsible for oxygen sensing, may serve as key regulators in causing IH-
dependent changes associated with AD. We hypothesize that IH-dependent activity from the carotid bodies,
causes oxidative stress, which in turn, promotes neurodegeneration and facilitates neuropathologies
associated with AD. To test this, we developed a set of aims that: (1) examines the role of carotid body
activity on hippocampal based-behavior and neurophysiology; and (2) determines how carotid body activity
influences neurodegeneration and plaque formation in an AD mouse model exposed to IH. By defining how
carotid body activity influences IH-dependent outcomes, our work establishes a new area of research that will
identify systemic mechanisms promoting neurodegeneration and neuropathological changes that drive
cognitive decline and dementia in AD. This work may lead to effective therapies needed to alleviate the burden
of AD and AD related dementias for millions of Americans suffering from the disease.

## Key facts

- **NIH application ID:** 10123911
- **Project number:** 3R01NS107421-03S1
- **Recipient organization:** UNIVERSITY OF CHICAGO
- **Principal Investigator:** Alfredo J Garcia
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $405,000
- **Award type:** 3
- **Project period:** 2018-05-01 → 2023-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10123911

## Citation

> US National Institutes of Health, RePORTER application 10123911, Neurocognitive Consequences of Intermittent Hypoxia (3R01NS107421-03S1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10123911. Licensed CC0.

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