A common epilepsy drug shows promise in Alzheimer’s prevention
A study in *Science Translational Medicine* reveals that levetiracetam, a widely used anti-seizure medication, can prevent the production of amyloid-beta (Aβ) in models of Alzheimer’s disease. The drug works by binding to the synaptic vesicle protein SV2a, which in turn modulates the processing of amyloid precursor protein (APP) away from the amyloidogenic pathway. This finding suggests a novel, repurposable mechanism for targeting a core pathological process in Alzheimer’s.
Why it might matter to you:
This research bridges neuropharmacology and neurodegenerative disease, demonstrating how a drug with a known neurological target can influence protein processing central to dementia. For a researcher in neurodevelopmental disorders, it underscores the importance of synaptic proteins and vesicular trafficking in broader neuropathology, potentially revealing common mechanistic pathways. It also highlights a strategy for drug repurposing that could be relevant for investigating therapeutic avenues in other complex neurological conditions.
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