These findings suggested that AEVs secreted in the AD brain (AEVs-Aβ) did not ameliorate Alzheimer's phenotype while AEVs modified by aFGF stimulation in Aβ-loading condition (AEVs-Aβ+H) attenuated the cognitive behavior deficits and Aβ burden accompanied with improved neurite growth and synaptic stabilization. Here, FGF1 is linked to Alzheimer disease.