ABSTRACT: β-Amyloid (AB) peptides are most likely involved in the neurodegenerative process occurring in Alzheimer's disease (AD) and are enriched in senile plaques. The mechanisms of Aβ toxicity are not clear but likely involve free radicals and apoptosis. Much interest is currently aiming at developing effective approaches to block Aβ toxicity in order to slow down disease progression. In that context, we are particularly interested in studying the role of insulin-like growth factors, particularly IGF-I and purported free radical scavengers including a Gingko biloba extract (EGB761) as blocker of Aβ toxicity in a simple in vitro model of hippocampal primary cultures. We observed that both IGF-I and EGB761 are unique in that they are able not only to protect but even to rescue neurons against Aβ toxicity. These results are summarized here and possible mechanisms of action are discussed to explain the protective properties of these two classes of agents.