How low oxygen and genetic tweaks may repair mitochondrial problems linked to Alzheimer’s and other disorders
Official title: Molecular mechanisms of mitochondrial complex I rescue by hypoxia and genetic suppressors
Funded at Brandeis University · NIH-11440919 · Data updated 2026-11-12
A Johns Hopkins-style? (Note: institution specified later) patient-facing overview: researchers will study tiny cell power stations in mitochondria to see if low-oxygen conditions and specific genetic changes can fix problems associated with Alzheimer's disease and related dementias.
Quick facts
| Grant type | R21 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Brandeis University NIH-funded |
| Lab location | 1 site (Waltham, United States) |
| Project start | September 1, 2026 |
| Project end | August 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $436,864 |
| NIH project number | 1R21NS151350-01 |
| Project ID | NIH-11440919 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with Alzheimer’s disease, Alzheimer’s-related dementia, or related neurodegenerative conditions could benefit from future therapies inspired by this research.
✕Less likely to help
Current patients should not expect immediate treatments from this early-stage study.
What this research studies
This project looks at mitochondrial complex I, a key part of cellular energy, and how reducing oxygen levels or using genetic changes might stabilize it to prevent nerve cell damage seen in Alzheimer’s and related conditions. The team will use fruit worm models and mouse studies along with advanced imaging to watch how the molecular machines rearrange themselves under hypoxia. By comparing normal and altered versions of complex I, they aim to map exactly how these conditions improve function and reduce harmful processes. The findings could point to new ways to protect brain cells from degeneration. The work combines genetics, biochemistry, and high-resolution structure technology to connect basic biology with potential therapies.
Why it matters
Potential benefit: If successful, this work could reveal new targets to protect brain cells in Alzheimer’s disease and other neurodegenerative conditions.
How similar studies have gone: Early studies in model organisms show that hypoxia can modify mitochondrial function, but the exact human-relevant mechanisms are still being explored.
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.