Investigating the role of microRNA210 in brain inflammation after ischemic stroke
Official title: MicroRNA210 and neuroinflammation in acute brain injury of ischemic Stroke
Funded at Loma Linda University · NIH-10579511 · Data updated 2026-11-12
This study is looking at how a tiny molecule called microRNA210 affects inflammation in the brain after a stroke, with the goal of finding new ways to help stroke patients recover better.
Quick facts
| Grant type | R21 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Loma Linda University NIH-funded |
| Lab location | 1 site (Loma Linda, UNITED STATES) |
| Project start | December 15, 2022 |
| Project end | November 30, 2025 |
| Funding year | 2023 |
| Award (this year) | $443,438 |
| NIH project number | 1R21NS126583-01A1 |
| Project ID | NIH-10579511 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for this research are individuals who have experienced an ischemic stroke and are facing challenges related to brain injury and inflammation.
✕Less likely to help
Patients who have not experienced an ischemic stroke or have other unrelated neurological conditions may not benefit from this research.
What this research studies
This research focuses on understanding how microRNA210 influences neuroinflammation in the context of acute ischemic stroke. The study aims to explore the molecular mechanisms behind brain injury and inflammation, particularly how microglial cells respond to ischemic conditions. By examining the effects of inhibiting microRNA210, researchers hope to identify new therapeutic targets that could lead to more effective treatments for stroke patients. The approach includes both laboratory experiments and analysis of inflammatory responses in brain cells.
Why it matters
Potential benefit: If successful, this research could lead to new therapies that reduce brain inflammation and improve recovery outcomes for stroke patients.
How similar studies have gone: Previous research has shown promising results in targeting neuroinflammation for stroke treatment, suggesting that this approach could be beneficial.
Where this research is happening
-
Loma Linda University
Loma Linda, United States Active
Researchers
- Principal investigator: Ma, Qingyi — Loma Linda University
- Study coordinator: Ma, Qingyi
Related research
Other NIH-funded projects on the same topics.
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Understanding how high homocysteine levels worsen brain injury after a stroke
This research looks at how high levels of a substance called homocysteine in the blood might make brain damage worse for people who have had an ischemic stroke.
-
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.
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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.
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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.
-
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.
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.