Scientists at the University of Arizona have discovered a potential new treatment to reduce the risk of post-stroke dementia.
The researchers investigated the chemical cyclodextrin, which can gather and safely store cholesterol without triggering a heightened inflammatory response.
In the study, treatment with cyclodextrin resulted in less inflammation and cholesterol accumulation within the brain of animal models.
The chemical also protected memory function, reduced neurodegeneration and reduced impulsivity, a personality change that can occur after stroke.
Lead investigator Kristian Doyle, PhD, an associate professor of immunobiology at the UArizona College of Medicine, said:
“Cyclodextrin helped remove cholesterol derived from the breakdown of dead brain cells, dampen inflammation and improve recovery.”
After an ischemic stroke occurs, immune cells remove the remnants of dead or damage blood cells and begin the healing process.
However, when this inflammatory response is prolonged, it can damage healthy tissue.
The inflammation can last for months as the high level of cholesterol in brain cells is difficult for immune cells to remove.
This process attracts more immune cells, elevating and prolonging the response and damaging healthy brain cells.
Dr Doyle said:
“Up to one-third of people who have a stroke develop dementia in the months afterward. We don’t know what causes that.
“We’ve been testing the hypothesis that, in some people, dementia could be caused by a lingering, smouldering inflammatory response at the site of the stroke, causing further damage to neighbouring brain regions.
“A promising target for enhancing recovery is to quench the inflammatory response sooner.”
Post-stroke dementia will typically set in within three to six months, according to the Alzheimer’s Society.
These individuals will typically experience vascular dementia.
Early signs of vascular dementia include forgetfulness, difficulty concentrating, feeling down or depressed and struggling to plan ahead.
