Overview
- In Science Translational Medicine, Northwestern scientists report that Aβ42 accumulates inside synaptic vesicles and that levetiracetam prevents its formation in mouse models, cultured human neurons, and high‑risk human brain tissue.
- The drug’s proposed mechanism involves SV2A binding that slows synaptic vesicle recycling, keeping APP at the cell surface longer and diverting it from amyloidogenic processing.
- A correlative analysis of National Alzheimer’s Coordinating Center records found patients on levetiracetam had a modestly longer interval from cognitive decline diagnosis to death compared with peers on lorazepam or other anti‑epileptics.
- Authors say any benefit would likely require very early preventive use in high‑risk groups such as people with genetic forms of Alzheimer’s or Down syndrome, not after dementia has begun.
- Researchers caution that evidence is largely preclinical, the drug has a short half‑life, longer‑lasting analogs are in development, and controlled trials are needed to test dosing, timing, and relevance to sporadic late‑onset disease.