High-dose vitamin B1 (benfotiamine) to reduce harmful sugar-related protein damage in Alzheimer's
Official title: Mechanistic links between the benefits of pharmacologically high thiamine (vitamin B1) in Alzheimer's disease to Advanced Glycation Endproducts (AGE)
Funded at Winifred Masterson Burke Med Res Inst · NIH-11258969 · Data updated 2026-11-12
Looks at whether high-dose thiamine (benfotiamine) lowers harmful sugar-related protein damage and helps people with Alzheimer's, and whether the common APOE4 gene changes the effect.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Winifred Masterson Burke Med Res Inst NIH-funded |
| Lab location | 1 site (White Plains, United States) |
| Project start | February 1, 2024 |
| Project end | January 31, 2029 |
| Funding year | 2026 |
| Award (this year) | $1,557,123 |
| NIH project number | 5R01AG082228-03 |
| Project ID | NIH-11258969 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal participants are people with Alzheimer's disease or related cognitive impairment who can provide blood samples and clinical information, and who can be genotyped for APOE.
✕Less likely to help
People who carry the APOE4 gene may get less benefit based on prior results, so they might not experience the same effects.
What this research studies
This project follows up on a small clinical finding that benfotiamine (a form of vitamin B1) lowered blood markers called advanced glycation endproducts (AGE) and improved symptoms in some people with Alzheimer’s. Researchers will map which proteins and exact sites are modified by AGE and test how high thiamine changes those modifications. The team will compare results between people with and without the APOE4 genetic risk to understand why APOE4 carriers had smaller benefits previously. Outcomes come from lab analysis of patient-derived samples and linked clinical measures to see who may benefit most.
Why it matters
Potential benefit: If successful, this work could support a low-cost treatment approach using benfotiamine to reduce damaging AGE and slow Alzheimer's-related damage, and help target the therapy by APOE type.
How similar studies have gone: A prior small clinical trial showed reduced plasma AGE and symptom improvement with benfotiamine, but larger and more detailed mechanistic work is still needed.
Where this research is happening
-
Winifred Masterson Burke Med Res Inst
White Plains, United States Active
Researchers
- Principal investigator: Gibson, Gary E — Winifred Masterson Burke Med Res Inst
- Study coordinator: Gibson, Gary E
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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.