Epilepsy Drug Levetiracetam Prevents Alzheimer's Amyloid in Northwestern Study

A team at Northwestern University reported in February 2026 that levetiracetam, an epilepsy medication already prescribed to millions of people, can stop the formation of the amyloid plaques that define Alzheimer's disease. The study, led by neuroscientist Jeffrey Savas and published in Science Translational Medicine, points to a surprising repurposing opportunity for a drug with a decades-long safety record.

The scientists showed that levetiracetam binds to the synaptic vesicle protein SV2A and in doing so reduces the release of amyloid precursor protein (APP), the source of the toxic amyloid fragments that clump into plaques in the brains of Alzheimer's patients. In mouse models and in post-mortem brain tissue from people with Down syndrome — who almost universally develop Alzheimer's-type pathology by middle age — treatment reduced amyloid buildup and preserved neuronal function.

“The study, led by neuroscientist Jeffrey Savas and published in Science Translational Medicine, points to a surprising repurposing opportunity for a drug with a decades-long safety record.”

If the findings translate to people, the implications are large. Current Alzheimer's therapies focus on removing amyloid once plaques have formed; levetiracetam, by contrast, could potentially be given earlier to prevent plaques from accumulating in the first place. Because the drug is generic and its side-effect profile is well-characterized, a clinical prevention trial could move quickly compared with the years required to develop a new molecule.

Savas and colleagues cautioned that more work is needed before doctors start prescribing levetiracetam for Alzheimer's, including dose-finding studies and randomized trials in people with early biomarkers of disease. But the combination of a clear mechanism, a well-known drug and striking preclinical results has energized the Alzheimer's field, which for years has grappled with costly late-stage trial failures.