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 A beta formation can be regulated by various means. This raises the possibility that altered APP processing may cause an increase in A beta formation in AD, and suggests that it may be possible to regulate the production of A beta 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 A beta production, then decreasing A beta production should delay the onset of the disease. Even in individuals where increased A beta 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 A beta accumulation and hence synaptic loss, decreasing A beta 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.