Cerebrovascular diseases resulting in cerebral ischemia, including stroke and cardiac arrest, are sexually dimorphic, with women experiencing relative protection compared to men. The reduced incidence and improved outcome in women has been attributed to neuroprotection provided by the endogenous female sex steroids, in particular estrogen. Consistent with this hypothesis, incidence of brain attack significantly increases following menopause in women and the sex difference is minimized. Our laboratory has a long-standing interest in unraveling the signaling pathways involved in estrogen neuroprotection. Current projects in the laboratory are focused on identifying downstream effectors of novel membrane associated estrogen receptors (GPR30) as well as assessing the effect of age on estrogen signaling and neuroprotection. In particular we have developed novel models to study adolescent stroke and cardiac arrest as well as aging mouse studies.