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Neurodegenerative disorders steal years of healthy life more quietly than many diseases, but despite the enormous physical, emotional, and economic burdens, most funding still chases late-stage symptoms or exclusively focuses on care as opposed to prevention. We take a different view: the common thread across many dementias is brain aging itself. If we can slow, halt, or even reverse core aging processes in the brain, we could prevent multiple diseases at once.

The University of Copenhagen team, led by Prof. Morten Scheibye-Knudsen, is doing exactly that. Their project targets a quiet saboteur of brain health, but one with tremendous consequences: senescent cells. Senescent cells are worn-out cells that stop multiplying but don’t die. They hang around and release “stress signals” that can irritate nearby cells and tissues. They linger, inflaming their neighbourhood and disrupting healthy brain function. Clearing them, while protecting the neurons that store your memories and personality, could remove one of the root pressures that push the aging brain toward dementia. What makes us confident isn’t just the idea, it’s how the team plans to execute it. They are developing compounds designed to selectively remove senescent brain cells while sparing healthy neurons. To find those needles in a haystack, they use AI-driven screening to triage vast chemical spaces, then put the best candidates through rigorous testing to verify safety and specificity. In a field where blunt tools can do harm, this blend of smart discovery and careful validation is essential.

We compared this strategy with common paths in dementia research, such as boosting neurotransmitters for a temporary lift, clearing a single protein late in the disease, or relying on cognitive training while the underlying biology continues to deteriorate. Those efforts can help around the edges, but they rarely change the long-term trajectory. By contrast, clearing senescent cells could change the slope of brain aging itself, including less inflammation, healthier cellular neighbourhoods, and sturdier neural circuits, potentially lowering the risk or delaying the onset of neurodegenerative diseases like Alzheimer’s and other dementias.

If successful, this could become an affordable treatment available outside the hospital, perhaps in the form of a pill or an occasional dose, along with a simple test to identify who’s most likely to benefit. The potential impact of delaying neurodegeneration is immeasurable, and could lead to fewer emergency visits and hospital stays, lower costs for families and healthcare systems, and, most importantly, more good years for loved ones to remain themselves. And the need is urgent: globally, around 57 million people are living with dementia, with nearly 10 million new cases each year, roughly one every three seconds, and in the U.S. an estimated 7.2 million people aged 65+ are living with Alzheimer’s in 2025. On top of this, many cases go undiagnosed or are diagnosed late, which robs families of the chance to act early. This is the tide we’re working to turn.

Every family seems to have a version of the same story: a loved one who begins to misplace names, then days, then parts of themselves. Our mission is to fight that norm, and keep similar stories from materializing. This grant embodies the LSF’s philosophy: prevention-first, biology-first, and built for clear, near-term readouts that can move from lab bench to everyday life. When you donate to this work, you’re not only adding years to lifespan, but you’re protecting the person inside those years, including the memories, friendships, and everyday autonomy that make a life feel like your own. Join us to push dementia from “inevitable” to “avoidable,” and help return stolen time to the families who need it most.