# Alcohol Use Disorder and Associated Neurological Symptoms of Cognitive Dysfunction and Pain

> **NIH NIH P60** · LSU HEALTH SCIENCES CENTER · 2022 · $46,643

## Abstract

Abstract LSUHSC CARC Research Component 3: Alcohol Use Disorder & Associated Neurological
Symptoms of Cognitive Dysfunction and Pain
Alcohol use disorder (AUD) is characterized by neurological deficits, negative affective states, and a profound
escalation of drinking. The cognitive and behavioral deficits associated with excessive drinking are attributed to
functional and persistent changes to neuronal circuitry. Chronic alcohol induced-cognitive impairments are
associated with selective central nervous system damage in areas such as the prefrontal cortex (PFC).
Excessive alcohol exposure also damages the peripheral nervous system to produce a characteristic
neuropathy, and the resulting hyperalgesia (increased pain sensitivity) is hypothesized to potentiate negative
reinforcement processes to increase motivation for alcohol. Alcohol use also represents a major exacerbating
factor for human immunodeficiency virus (HIV) disease. Even in the post-antiretroviral therapy (ART) era
neurocognitive deficits remain prevalent in persons living with HIV (PLWH). HIV-associated neurocognitive
disorder (HAND) and co-occurring AUD can exacerbate these deficits. PLWH also suffer from chronic pain,
which disrupts physical and emotional function, interferes with ART adherence, and doubles the chance of
virologic failure. Pain symptoms in PLWH are associated with specific changes in the brain and correspondingly
associates with numerous psychosocial factors in this population, including depression. While cognitive deficits
and pain are closely linked in PLWH, few studies have examined the stress-related neurobiological factors that
drive these interactions or how alcohol and HIV promote this process. The PFC represents and executes the
highest forms of goal-directed behavior, and its function is compromised in motivational disorders such as AUD.
As a potential neurobiological correlate of pain and cognitive impairment in PLWH, preclinical studies from our
group and others have implicated a functional potentiation of glucocorticoid receptor (GR) signaling in
association with excessive alcohol drinking, cognitive dysfunction, and chronic pain. Heightened GR signaling
and altered excitability of vulnerable cognition- and pain-related brain areas such as the PFC may thus represent
a unifying mechanism contributing to these pathologies. Finally, emerging evidence suggests that Western diets
commonly consumed in the United States worsen both neurocognitive and pain symptomatology. Thus, the
neurobiological interaction of excessive alcohol drinking, cognition, and pain in the context of Western diet
consumption represents a critically underexplored area of HIV research in the public interest. Our overarching
hypothesis is that excessive drinking and HIV/ART exposure in individuals consuming a Western diet additively
produce cognitive deficits and hyperalgesia in PLWH in association with increased glucocorticoid signaling and
hyperexcitability within the PFC. We will exam...

## Key facts

- **NIH application ID:** 10310696
- **Project number:** 5P60AA009803-29
- **Recipient organization:** LSU HEALTH SCIENCES CENTER
- **Principal Investigator:** Scott Edwards
- **Activity code:** P60 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $46,643
- **Award type:** 5
- **Project period:** 1996-12-01 → 2024-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10310696

## Citation

> US National Institutes of Health, RePORTER application 10310696, Alcohol Use Disorder and Associated Neurological Symptoms of Cognitive Dysfunction and Pain (5P60AA009803-29). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10310696. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*