Leaking mitochondrial DNA that turns on brain immune cells in Alzheimer's
Official title: mtDNA leakage and STING-dependent microglial innate immune response in Alzheimer's disease
Funded at Wake Forest University Health Sciences · NIH-11413325 · Data updated 2026-11-12
This research explains how fragments of mitochondrial DNA can switch on immune responses in the brain and contribute to inflammation in people with Alzheimer's.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Wake Forest University Health Sciences NIH-funded |
| Lab location | 1 site (Winston-Salem, United States) |
| Project start | January 15, 2022 |
| Project end | November 30, 2026 |
| Funding year | 2026 |
| Award (this year) | $474,886 |
| NIH project number | 7R01AG075108-05 |
| Project ID | NIH-11413325 on NIH RePORTER |
Who could benefit from this research
✓Could help
People diagnosed with Alzheimer's disease or mild cognitive impairment who can provide clinical samples or participate in related research at the study site.
✕Less likely to help
People without Alzheimer's-related neuroinflammation, those with other types of dementia, or anyone seeking immediate approved therapies are unlikely to receive direct clinical benefit from this laboratory-focused work.
What this research studies
Researchers will examine brain immune cells (microglia) from people with Alzheimer's and from an Alzheimer mouse model to see whether mitochondrial DNA leaks into the cell fluid and activates the cGAS–STING pathway. They will compare patient samples and animal tissues, measure mitochondrial DNA in microglia, and track markers of STING-driven inflammation. In mice, the team will reduce cGAS or block STING signaling to see if that lowers microglial inflammation and related brain damage. The goal is to find whether this pathway could be a target for treatments that reduce harmful inflammation in Alzheimer's.
Why it matters
Potential benefit: If successful, this work could point to new anti-inflammatory approaches that slow brain damage in Alzheimer's by blocking the cGAS–STING pathway.
How similar studies have gone: Preclinical studies have linked cGAS–STING to neuroinflammation and shown reduced inflammation when the pathway is blocked in animal models, but human therapies based on this approach remain experimental.
Where this research is happening
-
Wake Forest University Health Sciences
Winston-Salem, United States Active
Researchers
- Principal investigator: Du, Heng — Wake Forest University Health Sciences
- Study coordinator: Du, Heng
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About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.