University of New Mexico researchers have received federal funding to study how exposure to wildfire smoke creates signs of premature aging in the brain – and look for ways to inhibit the process.
Thanks to a five-year, $3.7 million grant from the National Institute on Aging and the National Institute of Environmental Health Sciences, a multi-disciplinary team led by Matthew Campen, PhD, MSPH, Regents’ professor in the UNM College of Pharmacy, will investigate how inhaled smoke particles travel from the lungs to erode the blood-brain barrier.
“We’ve had wildfires that are getting worse and worse,” Campen says. “We’ve been concerned about the acute changes that affect the brain, like neuroinflammation and loss of the blood-brain barrier. What are the long-term impacts? Could it promote Alzheimer’s and other forms of dementia?”
The study will combine Campen’s expertise in studying the cardiovascular effects of inhaled pollutants, with that of Alzheimer’s researcher Kiran Bhaskar, PhD, associate professor in the Department of Molecular Genetics & Microbiology, and Mark McCormick, PhD, assistant professor in the Department of Biochemistry & Molecular Biology, who studies the biology of aging. The project also includes colleagues at Virginia Commonwealth University and Florida International University.
A key question has to do with the role of inflammation in causing cells to age prematurely and become “senescent,” Campen says.
Cellular aging itself might be advanced by all this because you’re adding fuel to the fire when your cells become senescent
“Cellular aging itself might be advanced by all this because you’re adding fuel to the fire when your cells become senescent,” he says. “They start becoming inflammatory themselves. “We think senescent cells start releasing inflammatory cytokines that trigger other cells nearby to become senescent. Can wildfire smoke add to that?”
Campen and colleagues recently reported that airborne microscopic particles from woodsmoke can travel hundreds of miles and, when inhaled, cause toxic effects in the brain, even if they’re not sufficient to trigger respiratory symptoms. The risks are significant.
“You think of the millions of people in the western U.S. that have been exposed,” Campen says. The exposure could be triggering short-term impacts like depression and anxiety and long-term effects like the loss of healthy aging in the brain, he says.
The research also suggests that long-term exposure to particulates may help explain growing number of dementia cases in older Americans.
“Since 1970, we’ve done a great job of reducing air pollution,” Campen says. “But the ones alive back then are older and facing dementia. We don’t know how much of a risk we incurred as a result of that and how much of a risk are we still facing as a result of these other pollutants.”
Campen hastens to add that the study is not all doom and gloom.
“One of the bright sides of our grant is we are looking at certain interventions to see if we can inhibit some of the effects on the aging brain,” he says.
One approach focuses on resveratrol, a naturally occurring antioxidant compound found in the skins of grapes and blueberries that appears to protect the lining of the blood vessels. Older brains don’t metabolize resveratrol as well as younger ones, so the researchers will see whether combining it with another drug will enhance its effects.
Another arm of the study will focus on “senolytics,” drugs that remove senescent cells before they have a chance to trigger inflammatory effects in their neighbors. Removing damaged cells from the brain “strengthens the herd,” Campen says.