In 2010, a study found that AC can effectively cross the blood–brain barrier [16] and promote the expression of amyloid beta protein precursor (AβPP) and ADAM10 (a disintegrin and metalloproteinase 10), thereby driving the nonamyloidogenic pathway in neuroblastoma cells; in addition, it reduces the Aβ level in APP/PS-1 AD model mice [17] and it is thus regarded as one of the possible treatments for AD. This evidence concerns the gene ADAM10 and neuroblastoma.