This article reviews the relationship between brain aging and Alzheimer's disease (AD). Specific issues addressed include the question of whether AD and brain aging should be conceptually lumped or split, the extent to which AD and brain aging potentially share common molecular mechanisms, whether beta amyloid should be primarily considered a marker of AD or simply brain aging, and the definition of AD itself. A small percentage of individuals with normal antemortem psychometric scores meet the neuropathological criteria for AD termed "preclinical" AD (PCAD). PCAD and control subjects were compared for oxidative stress markers, amyloid beta-peptide, and identification of protein expression differences, and observed a significant increase in highly insoluble monomeric Aβ42, but no significant differences in oligomeric Aβ nor in oxidative stress measurements between controls and PCAD subjects. Expression proteomics identified proteins whose trends in PCAD are indicative of cellular protection, possibly correlating with previous studies showing no cell loss in PCAD.