Oxidative stress and the production of reactive oxygen species (ROS) has been implicated in a number of diseases associated with ageing, including Alzheimer’s disease (AD), atherosclerosis, rheumatoid arthritis and diabetes. An increase in oxidation products has been identified in Alzheimer’s pathology including DNA damage seen as an increase in 8-oxo-dG in cortical tissue and lymphocytes (1), markers of protein oxidation including protein carbonyl formation in Alzheimer’s brains (2) and plasma proteins of Alzheimer’s suffers (3). Dehydroepiandrosterone (DHEA) and its sulphate (DHEA-S) are hormones produced by the adrenal cortex. The levels of both are seen to decline in concentration with age. These levels have been associated with increased oxidative stress (4). Previous studies involving Alzheimer’s disease cell models have shown DHEA has antioxidant capabilities in protection of SH-SY5Y neuroblastoma cells against both direct oxidation reactions involving hydrogen peroxide and indirect radical attack via lipid peroxidation (5). A recent study was undertaken on 144 volunteers, (72 patients with AD, and 72 age matched healthy controls). AD sufferers had a decreased level of DHEA (4.24ng/ml ± 0.45 for control vs. 3.40ng/ml ± 0.34 in AD) which reached significance (p= 0.027, 1-tailed Mann Whitney). In addition results showed AD sufferers had a trend towards reduced DHEAS levels (0.90µg/ml ± 0.109 for control vs. 0.74µg/ml ± 0.078 in AD). DHEA levels were significantly correlated to DHEAS levels in both control and AD conditions (pearson correlation, r=0.641** control and r=0.618** AD; **p≤0.01). This study highlighted a measurable difference in DHEA and DHEA-S concentrations in plasma from patients suffering from AD when compared to age matched controls. This decrease may contribute to oxidative stress pathology in AD. The authors and others have shown that circulating DHEA levels increase following exercise, which may present opportunities for exercise interventions in populations where DHEA is reduced.