Understanding how the immune system removes synapses in Alzheimer's disease
Official title: Investigating Mechanisms of Complement Mediated Synaptic Removal
Funded at Henry Ford Health + Michigan State University Health Sciences · NIH-10889483 · Data updated 2026-11-12
This study is looking at how a part of the immune system affects brain connections in people with Alzheimer's disease, focusing on how certain proteins and inflammation might lead to memory loss, with the hope of finding new ways to help keep your thinking sharp.
Quick facts
| Grant type | R03 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Henry Ford Health + Michigan State University Health Sciences NIH-funded |
| Lab location | 1 site (East Lansing, United States) |
| Project start | August 15, 2024 |
| Project end | July 31, 2026 |
| Funding year | 2024 |
| Award (this year) | $314,000 |
| NIH project number | 1R03AG083563-01A1 |
| Project ID | NIH-10889483 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for this research are individuals diagnosed with early-stage Alzheimer's disease who are experiencing cognitive decline.
✕Less likely to help
Patients with advanced Alzheimer's disease or other forms of dementia unrelated to Alzheimer's may not benefit from this research.
What this research studies
This research investigates the role of the complement system, specifically complement C1q, in the removal of synapses in the brains of individuals with Alzheimer's disease. It aims to understand how pathological tau protein influences synaptic loss and how neuroinflammation may contribute to this process. By examining the mechanisms that lead to increased synaptic pruning, the study seeks to uncover potential targets for therapeutic intervention. Patients may benefit from insights that could lead to new treatments aimed at preserving cognitive function.
Why it matters
Potential benefit: If successful, this research could lead to new therapeutic strategies that slow down or prevent cognitive decline in Alzheimer's disease patients.
How similar studies have gone: Previous research has shown that targeting neuroinflammation and synaptic loss can lead to meaningful improvements in cognitive function in animal models, suggesting potential for success in human studies.
Where this research is happening
-
Henry Ford Health + Michigan State University Health Sciences
East Lansing, United States Active
Researchers
- Principal investigator: Benskey, Matthew John — Henry Ford Health + Michigan State University Health Sciences
- Study coordinator: Benskey, Matthew John
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.