The Vascular Side of Alzheimer’s Disease
Most Alzheimer's research focuses on plaques. Donna Wilcock's lab at IU School of Medicine is focused on what's happening in the blood vessels — and why it matters just as much.
Matthew Harris May 30, 2026
ALZHEIMER’S DISEASE IS more than plaques and proteins.
It’s also influenced by tiny blood vessels threaded through white matter — a network that ferries oxygen and nutrients that keep the brain working. When that system falters, the effects are harder to trace. Inflammation and immune cells can constrict those vessels or make them leak.
That’s where Donna Wilcock, PhD, and her team focus their research.
“Those cells are really good for our body to fight off infection,” said Wilcock, who is director of the Center for Neurodegenerative Disorders. “But those blood cells don’t belong in the brain, and when they get into the brain, they can do a lot of damage.”
Understanding why that happens has taken on new urgency.
In recent years, antibody therapies designed to clear hallmark amyloid plaques have become available. The drugs can slow disease progression, but their mechanism can strain fragile vessels. That can lead to swelling or small bleeds visible only on MRI, a condition called ARIA.
“It’s giving time back to patients,” said Erica Weekman, PhD, an assistant research professor of neurology who helps run Wilcock’s lab. “But with these kinds of therapies, you can have adverse vascular events.”
Those risks limit how many patients can receive the treatments.
Wilcock’s team is working to change that. Researchers are developing blood and retinal biomarkers to identify patients most at risk. They are also studying how inflammation weakens vessel walls, with the goal of protecting or stabilizing them.
A retinal biomarker, developed by Weekman, offers a simpler way to track vascular changes. Retinal vessels are part of the central nervous system, and changes there may reflect what’s happening in the brain. Imaging them — a routine part of an eye exam — is faster and less invasive than MRI.
“They can compare changes in those vessels to changes with ones in the brain,” Weekman said.
Wilcock’s lab also works across multiple models of Alzheimer’s, using cells, specialized mouse models and donated human tissue. “If we were looking to cure mice of Alzheimer’s, we’ve done that hundreds of times,” Wilcock said. “We need to make sure that whatever we’re looking at actually happens in the disease.”
Where that work happens shapes how quickly it moves.
Donna Wilcock, PhD, left, Malu Tansey, PhD, and Jason Meyer, PhD, in the Roberts Family Center for Alzheimer's Disease Research. High-end tools are pooled rather than duplicated — letting three teams do more, together, than any one lab could manage alone.
Last summer, Wilcock’s team moved into a lab on the 10th floor of the Medical Education and Research Building in Indianapolis. It houses tools to analyze samples on laser-thin slices of brain tissue. The space is shared with researchers Malu G. Tansey, PhD, and Jason Meyer, PhD, and was made possible by a $10 million gift from David and Susan Roberts.
Meyer’s group develops cellular models that replicate the brain’s vascular systems, while Tansey’s team studies how the immune system interacts with the brain. Those interests complement Wilcock’s work on vascular contributions to cognitive impairment and dementia.
Their labs form a continuous stretch of benches. The proximity enables techniques and troubleshooting to happen in real time. More importantly, it makes collaboration the default.
That approach extends to equipment. High-end tools are pooled rather than duplicated — from shared microscopy suites to imaging facilities — letting teams use more advanced systems than any one lab could support.
The Roberts family’s support helped build that system. Their gift funded key infrastructure, including a small-animal imaging facility, as well as the staff needed to run it effectively. The difference, Wilcock said, is not just having the equipment but being able to use it fully — allowing the team to do more, and to do it faster.
That speed matters because the problem is precise. Wilcock’s work on antibody therapies and vascular damage is a clear example of what the lab is trying to solve.
The therapies already work. The challenge is making them safer — focusing on the parts of the immune response that damage blood vessels without shutting down those that clear amyloid.
“We’re not trying to improve the immunotherapy,” Weekman said. “We’re trying to help stop some of these adverse events.”