Levetiracetam, an established antiepileptic medication, demonstrates a novel mechanism for preventing amyloid-beta 42 formation by altering how synaptic vesicles process the amyloid precursor protein. The drug binds to SV2a proteins and redirects APP toward non-toxic pathways, effectively reducing the peptides that form Alzheimer's characteristic plaques. Mass spectrometry validation confirmed this protective effect occurs in living brain tissue, not just laboratory cultures. This mechanism represents a significant departure from current Alzheimer's treatments, which primarily attempt to clear existing plaques rather than prevent their formation. The finding carries particular weight because levetiracetam already has FDA approval with established safety profiles, potentially accelerating clinical applications. Mouse models with aggressive amyloid pathology showed restored synaptic function and reduced neuronal loss when treated with the drug. However, the research remains in preclinical stages, and the dosing regimens that prove neuroprotective may differ substantially from current epilepsy protocols. The SV2a target also opens new therapeutic avenues, as other compounds affecting this protein could potentially offer similar amyloid-blocking effects with optimized pharmacological properties.