Levetiracetam May Halt Early Alzheimer's by Blocking Toxic Plaques

A study from Northwestern University suggests that levetiracetam, a widely used anticonvulsant, could halt the early onset of Alzheimer's disease by preventing toxic plaque formation and potentially restoring neuronal function.

Alzheimer's affects nearly 60 million people worldwide and remains incurable. The condition involves the buildup of toxic proteins in the brain, which disrupt neuron communication, trigger memory loss, dementia, and inflammation. Researchers at Northwestern University tested levetiracetam in animal models, human neurons, and brain tissue from high-risk patients. Their findings, published in *Science Translational Medicine*, indicate the drug acts as an early brake on disease progression.

The team focused on amyloid precursor protein (APP), which can follow one of two pathways: a harmless route or a harmful one producing beta-amyloid 42, a toxic fragment central to Alzheimer's initiation. Aging impairs the brain's ability to direct APP toward the safe path, boosting harmful production. Levetiracetam intervenes at this critical junction, steering APP away from the toxic route and blocking beta-amyloid 42 formation.

A key benefit is the drug's established safety profile. Approved decades ago for epilepsy treatment, it has a long track record in clinical use. Study authors view these results as validation for a new pharmacological target, bolstering efforts toward early prevention of neurodegenerative diseases.

While promising, the research remains experimental and has not yet advanced to human trials for Alzheimer's.