The team looked at 2-hydroxypropyl-β-cyclodextrin, or cyclodextrin, approved by the FDA for use as an ingredient in other drugs. Cyclodextrin’s chemical properties and shape allow it to safely “absorb” and store cholesterol without triggering an elevated inflammatory response.
Research shows that cyclodextrin treatment leads to less cholesterol accumulation and brain inflammation in animal models. Cyclodextrin also reduces neurodegeneration, protects memory function, and reduces impulsivity, a personality change that can occur after a stroke.
“Cyclodextrin helps remove cholesterol that is derived from the breakdown of dead brain cells,” said Kristian Doyle, an associate professor of immunobiology at UA Arizona College of Medicine – Tucson and the study’s principal investigator. , reduce inflammation and improve resilience.
An ischemic stroke occurs when blood vessels to the brain are blocked or limited, cutting off the brain’s supply of oxygen and nutrients and killing brain cells. The plaques of dead tissue that form promote inflammation, a normal process in which immune cells respond to the injured site to remove remnants of dead or damaged cells and initiate the process of cell death. healing process. However, when inflammation persists, it can damage healthy tissue.
In the case of a stroke, inflammation can last for months because brain cells contain a relatively high amount of cholesterol that is difficult for immune cells to get rid of. As immune cells struggle to process the accumulated cholesterol secreted by dead brain cells, they attract additional immune cells, elevating and prolonging the immune response, causing collateral damage. for healthy brain cells.
According to the World Health Organization, cerebrovascular accidents affect more than 15 million people around the world each year, and there is currently no cure.
“Up to a third of people who have a stroke develop dementia in the months that follow. We don’t know what causes that,” Dr. Doyle said. “We tested the hypothesis that, in some people, dementia may be caused by a persistent, insidious inflammatory response at the stroke site, causing additional damage to adjacent brain regions. One goal. promising to enhance recovery is quelling the inflammatory response earlier.”
Dr Doyle’s previous research showed that, after a stroke, the inflammatory response of dead brain tissue spreads to healthy brain regions, killing more brain cells.
“Immune cells rush in to clean up and repair, but they get overwhelmed and suck up other immune cells that make toxic substances to dispose of dead tissue. Unfortunately, these also damage the cells. damage areas not damaged by the initial stroke. Dr. Doyle said.
Dr Doyle, also a member of the BIO5 Institute, hopes future research will lead to the development of drugs that can improve recovery from stroke and reduce the risk of dementia after stroke. .
Co-authors include first author Danielle Becktel, a graduate student at the College of Medicine – Tucson, and Rick Schnellmann, PhD, UA Arizona College of Pharmacy dean R. Ken Coit and member of the BIO5 Institute .
Source: Eurekalert
