Therefore, the significant neuroprotective effect expressed in the inhibition of enzymes that impact the development of neurodegenerative diseases such as acetylcholinesterase, butyrylcholinesterase, and tyrosinase and the possibility of scavenging free radicals for caffeic acid from metal in-organic delivery systems can be extrapolated to in vivo conditions. This evidence concerns the gene ACHE and neurodegenerative disease.