One of the more prominent neurochemical defects in Alzheimer’s disease is a decrease in acetylcholine, associated with degeneration of basal forebrain cholinergic nuclei in most cases. The current prescription drugs approved for use in Alzheimer’s disease by the US Food and Drug Administration are acetylcholinesterase inhibitors. It was thought that another way to increase brain acetylcholine was administering precursors necessary for its synthesis. Phosphatidylcholine is a phospholipid that is the major dietary source of choline. Its administration increases levels of choline better than administration of choline by itself. Phosphatidylcholine is also crucial for cell membrane structure and function. Lecithin chemically is considered to be the same as phosphatidylcholine but when offered commercially it often refers to a mix of lipids that contain phosphatidylcholine. There have been a number of clinical trials of lecithin in Alzheimer’s disease, both as add-ons to clinical studies of tacrine, a cholinesterase inhibitor, and as studies of lecithin by itself. Theoretically it would appear to be difficult to increase brain acetylcholine by administering lecithin, because it is not a rate-limiting step in its synthesis. The lecithin studies as a group have not been particularly promising. A recent Cochrane review found no evidence to support the use of lecithin in Alzheimer’s disease105. Citicoline is another naturally occurring substance that is an intermediate metabolite in the synthesis of phosphatidylcholine. There have been phase III trials in stroke but only several short-term trials in older individuals and in those with dementia. The trials have been generally positive resulting in a Cochrane systematic review suggesting that there is some evidence of citicoline having a positive effect, at least in the short term106, although larger trials and those with longer duration are needed.