A model can be developed for familial APP mutation Alzheimer's disease to explain why a patient who is cognitively normal until middle age experiences a catastrophic amyloid deposition, which is to some extent mirrored in the clinical deterioration due to a subtle shift in A beta metabolism. However, the analysis of young onset dementia hardly constitutes the study of 'the suffering and infirmities of old age' which F E Williams' bequest is intended to promote. It remains to be seen whether the models relevant to APP mutation FAD can be applied to Alzheimer's disease of old age, or indeed other degenerative diseases of later life. Such models, however, do provide an alternative to the view that Alzheimer's disease is an incremental process virtually indistinguishable from old age itself. With an incremental linear process, treatment is akin to a war of attention. By contrast, with a catastrophic process the difference between a normal elderly person and a patient with incipient Alzheimer's disease at the start may be minimal, perhaps only a few molecules of extended A beta peptide, but they diverge very rapidly. If treatment can be directed at the metabolic events at the onset then there is a real opportunity for optimism. If ultimately successful, prevention rather than delay becomes a realistic goal, echoing Duc de La Rochefoucauld's desire 'to die as young as possible as late as possible'.