At the same time as Allen Roses and his colleagues were trying to convince the research community that APOE4 was implicated in increased risk of Alzheimer's disease, the pharmaceutical company Warner-Lambert was preparing to launch the first Alzheimer's drug treatment. Tacrine, as the product was called, is one of a family of compounds called acetyl cholinesterase (AChE) inhibitors, which delay the breakdown of the neurotransmitter acetylcholine, thought to have a central role in thought processes and memory function. The loss of the forebrain cholinergic system is characteristic of AD sufferers' brains; therefore it was supposed that AChE inhibitors would slow the development of symptoms of dementia.

These drugs have been around since the mid-nineteenth century, as variously: glaucoma treatment, insecticides, nerve gas and finally cognition enhancers (Taylor 1996). But, in a pattern which will be echoed later in this chapter, Tacrine's development was far from smooth. Initial claims about the drug's success in reducing the symptoms of AD were met with enthusiasm by other professionals, patients and family members (Summers et al. 1986; Herrman, Sadavoy & Steingart 1987). Over time however, questions were raised about the study's validity, with the US Food and Drug Administration (FDA) taking the unusual step in 1991 of publishing a report in the New England Journal of Medicine which was highly critical of the methods, assumptions and conclusions of the original study (FDA 1991).