Scientists at Northwestern University say a common anti-seizure medication may be able to prevent the earliest steps of Alzheimer’s disease—long before memory loss begins.
In a study published in Science Translational Medicine, researchers discovered how a particularly harmful protein linked to Alzheimer’s builds up inside brain cells.
Even more surprising, they found that levetiracetam, a decades-old and widely used anti-epileptic drug approved by the U.S. Food and Drug Administration, can block this process in laboratory models.
Alzheimer’s disease is known for the buildup of sticky protein clumps in the brain called amyloid plaques.
These plaques are largely made of a fragment called amyloid-beta 42, which is considered especially toxic to neurons.
While some newer drugs, such as lecanemab and donanemab, aim to clear plaques that have already formed, this new research focuses on stopping the toxic protein from being produced in the first place.
The team studied animal models, lab-grown human neurons, and brain tissue from people at high risk of developing Alzheimer’s.
They found that amyloid-beta 42 accumulates inside tiny structures in nerve cells called synaptic vesicles. These vesicles help neurons communicate with each other. When the researchers treated the cells and animals with levetiracetam, the drug prevented neurons from forming amyloid-beta 42.
The key lies in a protein called amyloid precursor protein, or APP. Normally, APP plays an important role in brain development and communication between nerve cells. But when it is processed in certain ways, it produces amyloid-beta fragments. The researchers discovered that levetiracetam changes how APP moves within neurons.
During the normal cycle of synaptic vesicles, levetiracetam binds to a protein called SV2A. This slows down the recycling of vesicle components inside the neuron. As a result, APP stays on the cell surface longer instead of being pulled inside the cell, where it would normally be processed into toxic amyloid-beta 42. By redirecting APP away from this harmful pathway, the drug reduces the production of plaques.
The researchers emphasize that this approach would only work very early—possibly decades before symptoms appear. By the time someone develops dementia, significant brain damage and cell death have already occurred. Therefore, levetiracetam would need to be taken long before memory problems begin, perhaps even 20 years earlier.
The team also analyzed existing clinical data from Alzheimer’s patients. They found that patients who happened to be taking levetiracetam showed a small but meaningful delay in disease progression compared to those not taking the drug or taking other seizure medications. While the effect was modest, it supports the idea that the drug may slow underlying disease processes.
The scientists also studied brain tissue from young adults with Down syndrome, who have a much higher risk of developing early Alzheimer’s due to extra copies of the APP gene. These brains showed early protein changes similar to those seen in experimental models, suggesting the drug might one day be tested as a preventive therapy in high-risk groups.
Researchers caution that levetiracetam is not a cure and is not ready for routine Alzheimer’s prevention. The drug breaks down quickly in the body, and scientists are now working to develop improved versions that last longer and target this mechanism more effectively.
Still, the findings offer new hope that preventing Alzheimer’s may be possible by intervening at the very earliest stages of disease—before plaques ever have a chance to form.
