APP processing appears to be under complex regulation. This regulation is apparently important under both normal and pathological conditions. Of direct clinical interest is the observation that Aβ formation can be regulated by various means. This raises the possibility that altered APP processing may cause an increase in Aβ formation in AD, and suggests that it may be possible to regulate the production of Aβ as a therapeutic approach in AD. As an example of the utility of the latter approach, consider a patient carrying the Swedish APP mutation. If it is true that the cause of AD in such a patient is due to increased Aβ production, then decreasing Aβ production should delay the onset of the disease. Even in individuals where increased Aβ formation is not the cause of AD but there is some other causes, such as the presence of an allele of apolipoprotein E which causes Aβ accumulation and hence synaptic loss, decreasing Aβ formation may be beneficial. It is of course a very long way from in vitro experiments to therapy. The current emphasis on studying APP processing in vivo represents the next step towards this goal.