Genes and environmental factors that can reduce mitochondrial damage
Official title: Identification of genetic and environmental suppressors of mitochondrial dysfunction
Funded at Brandeis University · NIH-11257672 · Data updated 2026-11-12
Researchers are looking for genes and environmental conditions that help damaged mitochondria work better, which may matter for Alzheimer’s and other brain conditions.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Brandeis University NIH-funded |
| Lab location | 1 site (Waltham, United States) |
| Project start | January 1, 2021 |
| Project end | December 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $249,000 |
| NIH project number | 5R00GM140217-04 |
| Project ID | NIH-11257672 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with Alzheimer’s disease, Parkinson’s disease, or inherited mitochondrial disorders would be the most relevant groups to benefit from follow-up therapies informed by this research.
✕Less likely to help
Patients whose symptoms are unrelated to mitochondrial dysfunction are unlikely to see direct benefits from this specific line of research.
What this research studies
From the patient perspective, scientists are using a tiny worm model to find genetic changes and environmental conditions that can counteract mitochondrial problems linked to Alzheimer’s and other diseases. They will test how low-oxygen exposure (hypoxia) and specific genetic changes restore mitochondrial function and study the biochemical steps involved. The team has already found several genetic “suppressors” in worms and will characterize how these work to inform human biology. While the work is done in the lab, the goal is to point toward targets or strategies that could later be tested in people.
Why it matters
Potential benefit: If successful, this work could point to new targets or strategies to protect brain cells and slow neurodegeneration in Alzheimer’s and some mitochondrial disorders.
How similar studies have gone: Prior lab studies in worms and other models have shown that hypoxia and certain genetic changes can rescue mitochondrial defects, although translating those findings to humans remains unproven.
Where this research is happening
-
Brandeis University
Waltham, United States Active
Researchers
- Principal investigator: Meisel, Joshua Daniel — Brandeis University
- Study coordinator: Meisel, Joshua Daniel
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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.