Amyloid plaques accumulate years before dementia, driven by release of the Aβ peptide from amyloid precursor protein (APP) in neurons. Now, new evidence points to synaptic vesicles as acidic hotspots that favor Aβ production. In the February 11 Science Translational Medicine, scientists led by Jeffrey Savas of Northwestern University in Chicago reported that Aβ42 and presynaptic proteins accumulate in Alzheimer’s mouse models and in young adults with Down’s syndrome. Further, they report that the FDA-approved anti-epileptic drug levetiracetam slows vesicle recycling and shifts APP toward the cell surface, reducing Aβ42 production.
