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Common Drug Could Stop Alzheimer’s Process ‘Before It Even Begins’

Levetiracetam slows synaptic vesicle cycling to reduce toxic amyloid-beta 42 production, potentially delaying early Alzheimer’s pathology by targeting presynaptic protein degradation, researchers say.

  • Now published in Science Translational Medicine, Northwestern University scientists report that levetiracetam prevents amyloid-beta 42 production and early plaque formation in Alzheimer’s models.
  • The researchers traced the cause to amyloid‑beta 42 accumulating in synaptic vesicles and impaired presynaptic protein degradation occurring early in amyloid pathology.
  • Laboratory experiments revealed that levetiracetam binds SV2A, slows synaptic vesicle cycling, increases APP cell-surface expression, and reduces amyloid plaque pathology and memory deficits in models.
  • Clinical data mining showed levetiracetam use linked to delayed decline-to-death in Alzheimer’s patients versus lorazepam, but its small benefit requires 'very, very early' use, possibly 20 years before detection.
  • Going forward, the team intends to develop longer‑lasting levetiracetam versions and target patients with Down syndrome, where more than 95% develop early Alzheimer’s, with clinical trials already underway.
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Levetiracetam prevents the formation of plaques associated with the disease, according to one study

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While anti-alzhéimer medicines remove existing plaques, anti-epileptic prevents the production of toxic beta-amyloid peptides

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Research suggests that this drug could act at very early stages of the disease, even decades before the first symptoms

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www.diariolibre.com broke the news in on Wednesday, February 11, 2026.
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