Researchers found that sialidase inhibitors—a class of flu drugs including oseltamivir (Tamiflu)—protected against degradation of protective sugar molecules tied to cognitive decline and premature aging in people living with HIV.
RT’s Three Key Takeaways:
- Glycan Degradation Mechanism: Researchers identified that the breakdown of protective sugar molecules, or glycans, triggers chronic inflammation and cognitive impairment in people living with HIV.
- Repurposing Flu Medications: Preclinical trials using sialidase inhibitors, such as oseltamivir, demonstrated that these drugs can preserve glycans and protect brain function by reducing biological aging.
- Gender-Specific Impact: The study found that women experience more rapid glycan degradation around menopause, suggesting that aging-related cognitive decline may accelerate differently across genders.
Northwestern University researchers have identified a biological mechanism that links the degradation of protective sugar molecules to cognitive decline and premature aging in people living with HIV, according to a study published in Med.
At least 25% of people living with HIV develop memory and thinking problems, even while receiving effective antiretroviral treatment. The study identified the degradation of protective sugar molecules, known as glycans, as a primary cause of these symptoms. When these molecules degrade, they fail to regulate inflammation, leading to chronic “inflammaging” that accelerates biological aging and causes the immune system to overreact.
Researchers analyzed blood samples from more than 100 individuals with HIV to identify the link between glycan patterns and cognitive impairment. In subsequent lab and mouse studies, the team found that sialidase inhibitors—a class of flu drugs including oseltamivir, also known as Tamiflu—preserved these sugar molecules and protected brain function.
“We are not saying yet that people should take flu drugs to prevent cognitive decline,” said Mohamed Abdel-Mohsen, associate professor of medicine in the division of infectious diseases at Northwestern University Feinberg School of Medicine, in a news release. “We are saying that our findings open the door to testing whether this drug class, or better next-generation versions, could be repurposed for brain and aging-related complications.”
The study utilized participants from the AIDS Clinical Trials Group, comparing those with normal cognition to those with clinical impairment. By blocking enzymes that typically degrade glycans, the flu drugs reduced inflammation, slowed biological aging, and protected memory in mouse models.
The research also highlighted gender differences in biological aging. While glycan degradation occurs steadily in men, it appears to accelerate in women around the time of menopause.
“Before menopause, women show a slower loss of anti-inflammatory glycans and slower accumulation of pro-inflammatory glycans compared with men, but around menopause there is a rapid shift toward a more inflammatory glycan profile,” said Abdel-Mohsen, who is also a member of Feinberg’s Potocsnak Longevity Institute, in a news release.
The team is currently working to optimize treatment strategies and determine if glycan levels can serve as blood biomarkers to predict future cognitive decline. The study received support from the National Institutes of Health (NIH) and the AIDS Clinical Trials Group.
