We have intertwined our interests in oxygen and the development of the central nervous and cardiovascular systems to propose that oxidative stress underlies the common molecular pathway via which prenatal hypoxia contributes to a developmental origin of both neurodegenerative and cardiovascular disease in adulthood, thereby explaining the high co-incidence of cardiovascular disease in patients with diseases involving memory impairment. The hypothesis will be tested in adult rat offpring of hypoxic or normoxic pregnancy with and without maternal antenatal antioxidant treatment using an integrative approach to analyse interactions within molecular and cellular networks that control whole animal cardiovascular physiology and behaviour.
