As with potential neurotransmitter therapy, the question of how successful reducing amyloid deposits would be in the treatment of Alzheimer's disease hinges on the position of amyloid formation in the pathological cascade. Identification of the presence of A4 reactive plaques and neurofibrillary tangles, either separately or together, in an increasingly wide variety of distinct diseases strongly suggests amyloid formation is "downline" in a variety of pathological processes. Thus, there may be no reason to expect amyloid therapy to be more effective than, say, transmitter therapy and, in view of the fact that neurodegeneration probably occurs in conjunction with amyloid formation, both therapeutic approaches should perhaps be considered together until such time as the primary etiopathological event is identified.