Why Alzheimer’s patients forget loved ones, and how UVA researchers are fighting back

November 6, 2025
illustration of 3 instant camera photographs depicting an MRI scan of a brain flanked by two blurry photos of couples

UVA researchers are studying how changes in the brain may cause Alzheimer’s patients to forget loved ones, and exploring new ways to prevent memory loss. (Illustration by John DiJulio, University Communications)

Few moments are more heartbreaking for families of Alzheimer’s disease patients than when a loved one no longer recognizes them. New research from the University of Virginia School of Medicine may reveal why that happens and offer hope for prevention.

UVA’s Harald Sontheimer, graduate student Lata Chaunsali and their colleagues found that when protective structures around brain cells break down, people may lose the ability to recognize loved ones. In lab studies, keeping these structures intact helped mice remember one another.

Harald Sontheimer looking at the camera through some laboratory shelves.

Harald Sontheimer chairs UVA’s Department of Neuroscience and is a member of the UVA Brain Institute. (University Communications photo)

“Finding a structural change that explains a specific memory loss in Alzheimer’s is very exciting,” said Sontheimer, chair of UVA’s Department of Neuroscience and member of the UVA Brain Institute. “It is a completely new target, and we already have suitable drug candidates in hand.”

A growing threat

Alzheimer’s disease affects 55 million people around the world, and that number is expected to grow by 35% in the next five years alone. In response, UVA has established the Harrison Family Translational Research Center in Alzheimer’s and Neurodegenerative Diseases as part of its Paul and Diane Manning Institute of Biotechnology.

The institute aims to accelerate the development of new treatments and cures for some of the world’s most challenging diseases, including Alzheimer’s.

Sontheimer’s research offers insight into how the disease develops. He and his team previously revealed the importance of what are called “perineuronal nets” in the brain. These nets act as protective barriers, ensuring nerve cells communicate properly. This communication is essential for neurons to form and store new memories.

Building on their earlier findings, Sontheimer and his collaborators suspected that disruptions in these protective nets might mark a critical turning point in Alzheimer’s disease. Their latest research supports that theory.

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Poster of advertisement written Faherty Tailgate Tour, Nov 7, 12-5PM, Nameless Field

Lab mice with damaged nets lost their “social memory” or the ability to recognize familiar mice, even though they could still form new memories and distinguish between familiar objects in their surroundings. This pattern closely mirrors what happens in people with Alzheimer’s, where social memory often fades before object memory.

Promising results

Sontheimer and his team, with support from the National Institutes of Health, the Owens Family Foundation, a Wagner fellowship and a Double Hoo fellowship, tested whether MMP inhibitors – a class of drugs already being studied for their potential to treat cancer and arthritis – could prevent the loss of the perineuronal nets. The treatment worked, preventing further damage and helping the mice keep their memories of one another.

“In our research with mice, when we kept these brain structures safe early in life, the mice suffering from this disease were better at remembering their social interactions,” Chaunsali said. “Our research will help us get closer to finding a new, nontraditional way to treat or, better yet, prevent Alzheimer’s disease, something that is much needed today.”

Turning these discoveries into a treatment will take time and further study, but Sontheimer and Chaunsali are optimistic.

“Although we have drugs that can delay the loss of perineuronal nets, and thereby delay memory loss in disease, more research needs to be done regarding safety and effectiveness of our approach before this can be considered in humans,” Sontheimer said.

“One of the most interesting aspects of our research is the fact that the loss of perineuronal nets observed in our studies occurred completely independent of amyloid and plaque pathology, adding to the suspicion that those protein aggregates may not be causal of disease.”

Media Contacts

Traci Hale

Senior Editor University Communications

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