A new drug target for Alzheimer’s emerges from an epilepsy treatment
A study in Science Translational Medicine reveals that levetiracetam, a common anti-seizure medication, can prevent the production of amyloid-beta (Aβ) peptides in models of Alzheimer’s disease. The mechanism is dependent on the drug binding to its known target, the synaptic vesicle protein SV2a. This interaction appears to modulate the processing of amyloid precursor protein (APP), reducing the generation of the pathogenic Aβ fragments that are central to Alzheimer’s pathology.
Why it might matter to you:
This finding directly connects a clinically approved drug to a core pathological pathway in Alzheimer’s, offering a novel and immediately testable therapeutic strategy. For your work on blood-based biomarkers, understanding how SV2a modulation alters APP processing could reveal new, druggable protein signatures in plasma that reflect target engagement or disease modification, moving beyond mere correlation to mechanistic insight.
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