Infections, cell aging, and the blood–brain barrier in Alzheimer's
Pathogen-induced cellular senescence and blood-brain barrier dysfunction in Alzheimer's Disease
This project looks at whether infections cause cells that line brain blood vessels to age and leak, potentially speeding Alzheimer's in people with or at risk for the disease.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Illinois at Chicago NIH-funded |
| Lab location | 1 site (Chicago, UNITED STATES) |
| Project ID | NIH-11248825 on NIH RePORTER |
What this research studies
From a patient's perspective, researchers will examine cells that make up the blood–brain barrier in Alzheimer's brains and in laboratory models to see if bacteria or viruses trigger premature cell aging (senescence). They will use single-cell gene profiling and a new computer tool called SenePy to identify senescent cells and inflammatory signals, including activation of endogenous retroviruses. The team will combine data from patient-derived samples and experimental models to link infection-driven inflammation with blood–brain barrier breakdown and Alzheimer’s-related changes. Findings will focus on molecular steps that could explain how airway or other infections might worsen cognitive decline.
Who could benefit from this research
Good fit: Ideal participants would include people with Alzheimer's disease, mild cognitive impairment, or older adults at higher risk of Alzheimer's, especially those with recent or repeated airway infections.
Not a fit: People without neurodegenerative disease or those whose dementia is driven solely by non-vascular mechanisms may be less likely to benefit directly from this work.
Why it matters
Potential benefit: If successful, this work could point to new ways to protect the blood–brain barrier or treat infection-driven inflammation to slow or prevent Alzheimer's progression.
How similar studies have performed: Previous studies have linked infections and blood–brain barrier damage to higher Alzheimer's risk, but applying single-cell senescence analysis and endogenous retrovirus signaling together is a newer and less-tested approach.
Where this research is happening
Chicago, UNITED STATES
- University of Illinois at Chicago — Chicago, United States (Active)
Researchers
- Principal investigator: Rehman, Jalees — University of Illinois at Chicago
- Study coordinator: Rehman, Jalees
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 below.