Can we afford to develop treatments for dementia?

his issue and that of the BMJ (22nd June 2002), are dedicated to neuro-degenerative disorders. We have come a long way in this field over the past two decades or so. Twenty years ago we knew only that Alzheimer's disease (AD) affected many elderly people, segregated in some early onset families, and was predominantly a disorder of cholin-ergic function. Now we have five years of postlicencing experience with the first drugs designed to rectify that cholinergic deficit 1 and our understanding of the molecular basis of AD is, if not complete, pretty much understood in outline. We know how the amyloid of plaques is produced in some detail and in the case of early onset familial AD we know why. 2 For late onset AD the influences on amy-loid formation, aggregation, and deposi-tion are less well understood, but we do know of some environmental influences such as head injury 3 4 and some genetic ones such as an as yet unidentified gene on chromosome 10. 5 We know about the aggregation of tau into tangles and, although the debate continues as to whether phosphorylation is primary or secondary, 6 some intriguing data indicate that it is this phosphorylation that underlies amyloid toxicity. 7 8. All of this hugely exciting research is leading to better understanding of the relation between the different demen-tias. We know, for example, that tau pathology is at the root of the frontotem-poral disorders and not just AD, 9 and that a complex relation exists between the previously distinct vascular dementia and AD. 10 We understand something of the molecular biology of Parkinson's disease and the accumulation of synuclein into Lewy bodies 11 —an understanding that is changing the way we think about the nosology of neurodegeneration. Despite these advances, much remains unknown. The advances in the understanding of the molecular biology of AD have not yet been matched by understanding of the molecular pathology of either motor neurone disease or Parkin-son's disease, although work on neuro-filaments and superoxide in relation to the former and synuclein and parkin in relation to the latter holds promise. Two of the big unanswered questions regarding neurodegeneration are why then, and why there? Why are there disorders of such late onset and what underlies the neuroanatomical and cellular specificity of disease? What relates genotype to pathology to phenotype? However, what really remains to be done is to cure the condition. New …