Current views associate the reappearance of cell cycle markers with early events in Alzheimer's disease. Even though, the cell cycle was implicated early in the study of this disease, only recently has it been associated with selective early vulnerability of neurons. The pathological hallmarks of Alzheimer's disease namely tau and amyloid have been associated with having effects on or being affected by cell cycle progression. Indeed the mitogenic component looms large early in the onset of Alzheimer's disease. Although quite a number of markers of reentry have been catalogued, the common denominator is abortosis, the unalterable march towards neuronal dysfunction, stasis and eventually death. We feel that complete understanding of the mechanisms, acting either positively by stimulation or through removal of inhibitory signals will provide promising molecular targets for pharmacological interventions which have been static for a number of years by being relegated to inhibition of the enzyme cholinesterase. In our opinion, investigating more proximal mechanisms will provide answers to changing the natural course of this illness.