Northwestern University researchers found that levetiracetam, an anti-seizure medication approved by the FDA in November 1999 under the brand name Keppra, may help prevent Alzheimer’s disease by blocking the formation of toxic amyloid beta peptides. The study, published in Science Translational Medicine, suggests the medication prevents the formation of amyloid-beta 42 in animal models, cultured human neurons, and post-mortem human brain tissue from individuals with Down syndrome, who are at high risk for Alzheimer’s.
Mechanism and Prevention Approach
The medication works through a distinct mechanism compared to existing Alzheimer’s drugs. While drugs such as lecanemab and donanemab are approved to clear existing amyloid plaques, levetiracetam prevents production of the amyloid-beta 42 peptides and plaques themselves. According to Jeffrey Savas, associate professor of behavioral neurology at Northwestern University Feinberg School of Medicine, “our new results uncovered new biology while also opening doors for new drug targets.” The brain normally avoids the pathway that produces toxic amyloid-beta 42 proteins in younger years, but the aging process gradually weakens that ability, Savas noted. In brains developing Alzheimer’s, too many neurons go astray and produce amyloid-beta 42, which then leads to tau (abnormal protein clumps inside neurons) that can kill brain cells, trigger neuroinflammation, and lead to dementia.
Critical Timing Requirements and Limitations
For levetiracetam to function as an Alzheimer’s prevention tool, high-risk patients would need to start taking it “very, very early”—potentially up to 20 years before elevated amyloid-beta 42 levels would be detected. Savas noted that the medication “is not perfect” and “breaks down in the body very quickly.” When researchers examined previous human clinical data, they reported that Alzheimer’s patients taking the anti-seizure drug had a “significant delay” in the span from cognitive decline to death, though Savas acknowledged the magnitude of change was small, “on the scale of a few years.” Common side effects include drowsiness, weakness, dizziness, irritability, headache, and loss of appetite. The medication has also been linked to potential mood and behavior changes, and in rare cases could lead to severe allergic reactions or suicidal ideation. The study was limited by reliance on animal models and cultured cells, with no human trials conducted.
This article is an AI-assisted summary. All facts and figures are drawn from the original report: https://www.foxnews.com/health/alzheimers-prevention-breakthrough-found-decades-old-seizure-drug