Understanding how cholesterol affects brain damage after a stroke
Official title: The role of cholesterol metabolic enzyme CYP46A1 and its metabolite 24S-hydroxycholesterol in ischemic stroke.
Funded at Morehouse School of Medicine · NIH-11143930 · Data updated 2026-11-12
This research explores how a cholesterol-related process in the brain contributes to damage after an ischemic stroke.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Morehouse School of Medicine NIH-funded |
| Lab location | 1 site (Atlanta, United States) |
| Project start | June 1, 2022 |
| Project end | May 31, 2027 |
| Funding year | 2025 |
| Award (this year) | $355,000 |
| NIH project number | 5R01NS128018-04 |
| Project ID | NIH-11143930 on NIH RePORTER |
Who could benefit from this research
✓Could help
This foundational research does not directly involve patient participation, but future clinical applications would target individuals at risk for or recovering from ischemic stroke.
✕Less likely to help
Patients not affected by ischemic stroke would not directly benefit from this specific research direction.
What this research studies
We are looking into how a specific cholesterol-processing enzyme, CYP46A1, and its product, 24S-hydroxycholesterol, impact brain injury following an ischemic stroke. Our main idea is that when CYP46A1 becomes more active, it creates more 24S-hydroxycholesterol, which then makes brain damage worse by affecting certain brain cell receptors. To understand this better, we are using laboratory models of stroke and advanced techniques to observe brain cell activity and calcium levels. This work aims to uncover the exact steps involved in how this cholesterol pathway contributes to stroke-related brain injury.
Why it matters
Potential benefit: If successful, this research could identify new targets for treatments to reduce brain damage and improve recovery after an ischemic stroke.
How similar studies have gone: While the role of cholesterol in stroke is an active area of investigation, this specific focus on CYP46A1 and 24S-hydroxycholesterol in ischemic brain injury represents a novel and untested approach.
Where this research is happening
-
Morehouse School of Medicine
Atlanta, United States Active
Researchers
- Principal investigator: Leng, Tiandong — Morehouse School of Medicine
- Study coordinator: Leng, Tiandong
Related research
Other NIH-funded projects on the same topics.
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Improving blood flow after stroke by breaking down NETs
Aims to see if breaking down neutrophil extracellular traps (NETs) after an ischemic stroke can improve blood flow and reduce brain injury in patients.
-
EP2 blockers to protect the brain after a stroke
Aims to test brain-permeable EP2 antagonists to reduce damage after ischemic stroke and improve recovery.
-
Genetic testing to find causes of early-onset ischemic stroke
This project uses whole-exome sequencing to look for gene changes that may cause ischemic stroke in adults who had a stroke at a young age.
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Targeted nanomedicine to protect the brain after stroke
A targeted drug-delivery approach aims to boost blood-brain barrier repair and reduce brain damage after an acute ischemic stroke in patients at risk.
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How biological aging and blood proteins relate to thinking after a stroke
This project looks at whether measures of biological aging and patterns of blood proteins help explain which stroke survivors keep their thinking sharp and which go on to develop vascular dementia.
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Repurposing NEXLETOL to treat ischemic stroke
Aims to see if the cholesterol drug NEXLETOL can help people after an ischemic stroke by supporting brain energy use and reducing injury.
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.