How increased IL-33 in the thalamus may worsen thinking problems after head injury in older adults
Official title: Influence of thalamic IL-33 signaling in aging-associated exacerbation of cognitive impairment after brain injury via microglial dysfunction and tau pathology
Funded at University of Alabama at Birmingham · NIH-11297674 · Data updated 2026-11-12
Researchers are seeing if higher IL‑33 signals in a deep brain area (the thalamus) help explain why older people have worse memory and thinking problems after a head injury.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Alabama at Birmingham NIH-funded |
| Lab location | 1 site (Birmingham, United States) |
| Project start | September 15, 2022 |
| Project end | June 30, 2027 |
| Funding year | 2025 |
| Award (this year) | $445,757 |
| NIH project number | 4R01AG079129-02 |
| Project ID | NIH-11297674 on NIH RePORTER |
Who could benefit from this research
✓Could help
Adults who are older and have had a traumatic brain injury or are worried about increased dementia risk after a head injury would be the most relevant group.
✕Less likely to help
People without a history of head injury or those with cognitive problems from unrelated causes (for example, stroke‑only injury or psychiatric conditions) are less likely to benefit directly from this line of research.
What this research studies
This work looks at how aging changes in the thalamus — especially a molecule called IL‑33 made by support cells — affect immune cells in the brain (microglia) and the buildup of abnormal tau protein after a head injury. In mice, the team causes controlled brain injury, compares younger and middle‑aged animals, and tests what happens when they block IL‑33 or alter microglia locally. They measure memory and thinking in the animals, examine brain tissue for tau and inflammation, and relate findings to human brain imaging that shows thalamic microglial activation. The goal is to connect age‑related molecular changes to worse cognitive outcomes after traumatic brain injury so new treatments can be identified.
Why it matters
Potential benefit: If successful, this could point to new ways to prevent or reduce dementia‑related decline after brain injury by targeting IL‑33 or microglial responses.
How similar studies have gone: Prior mouse experiments have shown that blocking IL‑33 or changing microglial activity can reduce tau buildup and improve cognition, but equivalent human treatments have not yet been proven.
Where this research is happening
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University of Alabama at Birmingham
Birmingham, United States Active
Researchers
- Principal investigator: Kano, Shinichi — University of Alabama at Birmingham
- Study coordinator: Kano, Shinichi
Related research
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Thalamic IL-33 signaling and aging-related cognitive decline after brain injury
Aiming to understand how aging and brain injury interact to worsen memory and thinking problems by studying a specific brain signal (IL-33) in the thalamus and its effect on brain immune cells and tau pathology.
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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.