At the moment there is no cure for Alzheimer's disease. The main problem is that we do not as yet know why particular cells in the brain degenerate whilst others do not. If we knew why certain populations of brain cells were vulnerable above and beyond the generic feature of being in the brain then we would be in a strong position to devise means of intercepting the process of continuing loss. In our group we have identified a mechanism that may be pivotal in Alzheimer's disease: the crucial process could be an aberrant recapitulation of normal development. We suggest that when this process is activated in the inappropriate context of the mature brain, then it proves toxic. More specifically we have demonstrated that brain cell populations primarily vulnerable in Alzheimer's disease have a defining characteristic: they all contain a certain substance that operates during development ubiquitously but which is retained selectively in these specific cell groups on into maturity. We suggest that when the mature cells are damaged they attempt to compensate by activating this key substance and that this proves lethal to the mature cells. In the first step towards developing a new therapy for arresting further cell death we have now identified the molecular target through which the substance acts. Our long term goal is therefore now to devise a test for detecting this substance during routine screens before the symptoms of Alzheimer's occur. If we were able to couple such a test with the prospect of a drug therapy that could intercept the action of the substance and thereby prevent further cell death, the symptoms would never appear! To this end we now need to explore the effects of the substance in the whole brain of rodents to see how the effects that we have studied in cell culture and slices of brain are reflected in behaviour. Not only will such work lead ideally to the development of a definitive "animal model" but as such it could provide the first crucial step in testing out the new therapeutic agents.