{"id":133698,"date":"2026-06-29T15:25:26","date_gmt":"2026-06-29T20:25:26","guid":{"rendered":"https:\/\/www.unmc.edu\/newsroom\/?p=133698"},"modified":"2026-06-29T15:25:28","modified_gmt":"2026-06-29T20:25:28","slug":"repurposing-hiv-drugs-to-fight-alzheimers","status":"publish","type":"post","link":"https:\/\/www.unmc.edu\/newsroom\/2026\/06\/29\/repurposing-hiv-drugs-to-fight-alzheimers\/","title":{"rendered":"Repurposing HIV drugs to fight Alzheimer’s"},"content":{"rendered":"
\n

Anna Frie didn’t set out to study Alzheimer’s disease. She set out to find the right lab.<\/p>\n\n\n\n

In October 2025, she rotated into the laboratory of Sowmya Yelamanchili, PhD, in the UNMC Department of Anesthesiology, drawn by the lab’s work building three-dimensional brain organoids.<\/p>\n\n\n\n

“I really enjoyed the people and the environment,” Frie said. “I decided it was where I wanted to spend my time in graduate school.”<\/p>\n\n\n\n

The science pulled her in just as much as the culture. Dr. Yelamanchili’s lab had existing expertise in HIV research, and Frie saw an opportunity to use that foundation to ask a new question: could drugs already approved to treat HIV also slow the progression of Alzheimer’s disease?<\/p>\n\n\n\n

At the center of Frie’s project is a molecular structure called the NLRP3 inflammasome \u2014 what she describes as the brain’s alarm system. Under normal circumstances, the inflammasome activates when cells sense damage. It triggers the release of an enzyme called caspase-1, which in turn releases an inflammatory signal called IL-1\u03b2. Short bursts of this response are healthy and necessary.<\/p>\n\n\n\n

In Alzheimer’s disease, however, the alarm never turns off.<\/p>\n\n\n\n

“The brain reads tau tangles and amyloid plaques as damage and keeps the alarm on,” Frie explained. “Releasing more IL-1\u03b2 causes even more tau and amyloid buildup. That sets up a self-reinforcing loop of inflammation driving neuronal damage and cognitive decline.”<\/p>\n\n\n\n

Breaking that loop is her goal.<\/p>\n\n\n\n

Rather than developing a new drug from scratch \u2014 a process that can take decades \u2014 Frie is investigating whether nucleoside reverse transcriptase inhibitors, or NRTIs, can do the job. NRTIs already are FDA-approved and have been used for years to treat HIV. Their safety profiles and side effects are well understood by clinicians.<\/p>\n\n\n\n

“If we can show that NRTIs reduce Alzheimer’s pathology, we’re using a drug that doctors already know how to prescribe safely,” Frie said. “Which gets us from the lab to patients faster.”<\/p>\n\n\n\n

Her project, titled “Leveraging antiviral drug repurposing to inhibit NLRP3-mediated neuroinflammation in Alzheimer’s disease,\u201d is in its early stages. She is currently working to identify early-onset Alzheimer’s cell lines to test with NRTIs that have been used previously in the Yelamanchili lab for HIV research. Success, she said, would look like data demonstrating that NRTIs disrupt the inflammatory loop driving tau aggregation and inflammasome activation \u2014 with the longer-term hope of testing the approach in brain organoids made from Alzheimer’s stem cells.<\/p>\n<\/a><\/div><\/div>","protected":false},"excerpt":{"rendered":"

Anna Frie is awarded the Nancy and Ronald Reagan Alzheimer’s Scholarship Award for her project titled “Leveraging antiviral drug repurposing to inhibit NLRP3-mediated neuroinflammation in Alzheimer’s 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