Protein build-up in brain blood vessels and dementia risk

In the US, health information of over 1.9 million adults aged 65 and older has led to suggested links between brain protein build-up and increased dementia risk.

People with cerebral amyloid angiopathy (CAA), a condition where protein (called amyloid) builds up in the brain, are four times more likely to develop dementia within five years, regardless of whether they have had a stroke. This is according to a preliminary study presented at the American Stroke Association’s International Stroke Conference 2026, which was held in February.

Some amyloid protein can collect in the brain’s blood vessels as people age and without causing symptoms. When the build-up becomes significant enough to damage the vessels and affect brain function, people receive a clinical diagnosis of CAA — a condition that raises the risk of ischemic stroke (clot-caused stroke) and can lead to haemorrhagic stroke (bleeding stroke).

Often found in people with Alzheimer’s Disease, CAA also contributes to cognitive impairment, and in some severe cases, the protein deposits can cause the walls of blood vessels to crack, which can lead to blood leaking out and damaging the brain — damage that is known as a bleeding or haemorrhagic stroke.

For this study, researchers investigated the risk of developing dementia among adults diagnosed with CAA, the link between CAA and stroke and the risk of dementia. “Many people with CAA develop dementia; however, so far, clinicians haven’t had clear, large-scale estimates on how often and how quickly dementia progresses in these patients,” said Samuel S. Bruce, M.D., M.A., study author and an Assistant Professor of Neurology at Weill Cornell Medicine in New York City.

“Our study calculated estimates from a large sample of Medicare patients whether people with CAA are more likely to be newly diagnosed with dementia and to clarify how CAA and stroke — separately and together — relate to new dementia diagnoses,” Bruce said. “What stood out was that the risk of developing dementia among those with CAA without stroke was similar to those with CAA with stroke, and both conditions had a higher increase in the incidence of dementia when compared to participants with stroke alone.

“This suggests that non-stroke-related mechanisms are instrumental to dementia risk in CAA,” Bruce said. “These results highlight the need to proactively screen for cognitive changes after a diagnosis of CAA and address risk factors to prevent further cognitive decline.” That researchers obtained clinical study information from administrative diagnosis codes used in inpatient and outpatient health insurance claims submitted to Medicare was among the study’s limitations. “These codes are an imperfect proxy for clinical diagnoses, and misclassifications can occur,” Bruce said.

Attempts by the researchers to mitigate the limitation included using codes that have been shown to accurately capture correct diagnoses in administrative data; though access to imaging data — to more rigorously assess the diagnoses of CAA and stroke — was not available. Prospective studies that follow patients forward (instead of looking back in time) are among the further research needed to confirm the results; studies should include standardised approaches for diagnosing CAA and stroke.

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