ABSTRACT
In a 1997 article entitled ‘Plundered Memories’, published in the now defunct journal The Sciences, Zaven Khachaturian, the Director of the Ronald and Nancy Reagan Research Institute of the Alzheimer’s Association had this to say:
In the same year, 1997, John Hardy, who researches the genetics of Alzheimer’s disease (AD), and is currently Chief of the Laboratory of Neurogenetics at the National Institute of Aging (NIA) of the US argued: ‘We now know several causes (emphasis added) of Alzheimer’s disease (all of them genetic).’ Hardy had in mind both early-onset AD, in which genes with an autosomally dominant mode of transmission are invariably involved, and late-onset AD in which the implicated susceptibility gene functions in a non-Mendelian manner and is estimated to be involved in only somewhere between 30 per cent and 60 per cent of the disease incidence. Hardy cannot be faulted for underestimating the complexity of action of this latter gene, given that his comment was made nearly a decade ago, and he went on to declare, ‘… The unofficial “goal” of the NIA is to have some form of effective therapy by the year 2000 and this goal may yet be realized’ (1997). At the time Hardy was perhaps justified in assuming that the new genetic insights could well bring about therapeutic advances but, as is well known, effective medication for AD has yet to be found, even though research into the genetics of dementia has accelerated exponentially since the end of the twentieth century.
