The brain targeting of quercetin-loaded exosomes enhanced its bioavailability in Alzheimer’s disease (AD) and further relieved the symptoms of AD via inhibition of biochemical pathways such as cyclin-dependent kinase 5 (CDK5)-mediated phosphorylation of phosphoprotein Tau and decrease of the formation of insoluble neurofibrillary tangles (NFTs) [116]. This evidence concerns the gene CDK5 and early-onset autosomal dominant Alzheimer disease.