A common anti-seizure medication, levetiracetam, may hold the key to preventing Alzheimer’s disease before symptoms even appear, according to new research from Northwestern University. Scientists have pinpointed when and where the toxic protein buildup that causes Alzheimer’s begins in the brain and discovered the decades-old drug can “stop” the process.
The research, conducted on February 14, 2026, identified that the protein beta-amyloid 42 accumulates inside synapses – the small packages used by nerve cells to send signals. Experiments using animal models, human cells, and brain tissue from individuals at risk revealed that levetiracetam prevents the formation of beta-amyloid 42 in nerve cells.
“While most current Alzheimer’s drugs aim to remove existing plaques, we’ve discovered a mechanism that prevents the production of beta-amyloid 42 proteins before they accumulate, offering new opportunities to develop preventative treatments,” said Jeffrey Savvas, associate professor of behavioral neuroscience at Feinberg School of Medicine, and the study’s lead author.
Researchers emphasize that early intervention – potentially 20 years before symptom onset – is crucial, particularly for those genetically predisposed to the disease, such as individuals with Down syndrome. Clinical data suggests that patients who took the medication experienced slower disease progression and lived longer after diagnosis.
The team is now working to develop an improved version of the drug that lasts longer in the body and more effectively targets this preventative mechanism. This discovery represents a significant step forward in the fight against Alzheimer’s, a disease that affects millions worldwide and for which there is currently no cure.
The study found the drug works by binding to a protein within the synapses, slowing their recycling process and diverting the APP protein away from the pathway that produces the toxic proteins. This finding offers a new avenue for research into preventative therapies for Alzheimer’s disease.
