HQ Team
November 20, 2025: All chronic illnesses are an emotional, physical and financial drain on the family. And when it is something like Alzheimer’s, the impact is shattering as one sees a loved one slowly fading away. The social amnesia —forgetting the very people who define our lives—cuts deepest. For decades, the infamous amyloid plaques were blamed for the disease, but scientists at the University of Virginia recently discovered the real culprit hiding in plain sight: microscopic “nets” around our brain cells, and they already know which drugs might save them.
Think of these nets as your brain’s memory cement. Called perineuronal nets, they’re web-like structures that wrap around neurons, locking in everything from your first kiss to your spouse’s face. When Alzheimer’s strikes, enzymes called MMPs chew through these nets like termites, dissolving the scaffolding that holds social memories in place. “In Alzheimer’s disease, people have trouble remembering their family and friends due to the loss of a memory known as social memory,” explains UVA grad student Lata Chaunsali, who co-authored the breakthrough study published in Alzheimer’s & Dementia.
Here’s the kicker: this net destruction happens completely independent of amyloid plaques. As senior author Harald Sontheimer bluntly puts it, this “adds to the suspicion that those protein aggregates may not be causal of disease.” In other words, scientists may have been following the wrong bad guy for twenty years.
The UVA team proved their theory in mice with faulty nets. The animals lost their ability to remember cage-mates while still forming object memories, perfectly mirroring human Alzheimer’s progression. But when they treated the mice with MMP inhibitors (drugs already in trials for cancer and arthritis), the nets stayed intact and social memory held strong. “We already have suitable drug candidates in hand,” Sontheimer says, which is scientist-speak for “this could move fast.”
UVA’s Alzheimer’s research has come up with another angle to tackle the disease. Dr John Lukens is taming an overactive immune molecule called STING that attacks the brain. His group found that deleting STING in mice prevented memory loss and reduced plaque buildup.
PHD candidate Jessica Thanos, who watched her grandmother fade from the disease, tested the mice in water mazes and saw dramatic improvements: “They seemed to learn much better and also remember the location information much better.”
In another study, Dr Lulu Jiang, who’s decoding the molecular whispers between RNA and tau protein, used 3D brain models to track how tiny RNA changes trigger the collapse of brain cell structure. “These hallmarks are present in the brain, but really the molecular mechanisms is unclear,” Jiang notes. Her five-year NIH grant could reveal the upstream signals that activate those net-destroying MMPs in the first place.
Hope vs. Reality
This does not mean that one can immediately march into any pharmacy and demand MMP inhibitors. Human trials are still years away. But with 55 million people globally living with Alzheimer’s, and nearly 20 million more projected diagnoses in the next five years, the urgency is crushing. The fact that these drugs already exist could slash a decade off development time.
For families watching loved ones slip away one face at a time, this isn’t just academic. The Harrison Family Translational Research Center at UVA is accelerating these discoveries precisely because they target what actually hurts most: losing each other. As Chaunsali says, “Our research will help us get closer to finding a new, non-traditional way to treat or better yet prevent Alzheimer’s disease—something that is much needed today.”
For the past twenty years, Alzheimer’s research has been a one-note amyloid obsession. Now it has moved into fresher territory of protect the nets, quiet the immune system, fix the RNA. So next time you hear about another failed amyloid drug, remember: the real story is unfolding in those tiny nets, the quieted immune molecules, and the RNA code-breakers. Your loved one’s face might not be lost forever after all.
