# Non-canonical cGAS signaling in DNA damage response

> **NIH NIH R01** · OHIO STATE UNIVERSITY · 2024 · $320,558

## Abstract

Project Summary:
Alzheimer's disease(AD) is the most prevalent form of dementia, accounting for approximately 60-70% of all
dementia cases worldwide. It has been increasingly recognized that NAD+ depletion and elevated activity of the
cGAS-STING pathway are implicated not only in normal aging but also in various neurodegenerative conditions,
including Alzheimer's disease. NAD+ metabolite plays a pivotal role in maintaining cellular homeostasis and is
considered one of the crucial hallmarks of aging and neurodegeneration. NAD+ depletion can trigger
mitochondrial dysfunction, inflammation, impaired lysosomal and proteasomal function, compromised adaptive
cellular stress responses, and hinder DNA repair mechanisms. Boosting NAD+ levels in animal models of AD
has been shown to ameliorate pathological features of AD. Interestingly our recent studies have demonstrated
that cGAS-STING activation induces NAD+ depletion in cell culture and mice. Considering this the novel
mechanistic link between cGAS-STING signaling and NAD+ depletion, we propose to gain insights into the novel
crosstalk between cGAS-STING pathways and NAD+ metabolism in the context of AD pathogenesis.

## Key facts

- **NIH application ID:** 10937475
- **Project number:** 3R01AI148741-05S1
- **Recipient organization:** OHIO STATE UNIVERSITY
- **Principal Investigator:** Nagaraj Kerur
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $320,558
- **Award type:** 3
- **Project period:** 2019-12-05 → 2025-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10937475

## Citation

> US National Institutes of Health, RePORTER application 10937475, Non-canonical cGAS signaling in DNA damage response (3R01AI148741-05S1). Retrieved via AI Analytics 2026-06-11 from https://api.ai-analytics.org/grant/nih/10937475. Licensed CC0.

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