Inhibition of age-induced beta-amyloid neurotoxicity in rat hippocampal cells.

The conditions under which beta-amyloid (Abeta) is toxic to primary rat hippocampal neurons were investigated. Synthetic Abeta(1-42) peptide was neurotoxic following "aging" for 7 to 14 days at 37 degrees C in modified Eagle's media. Neurotoxicity included decreases in neurite length, cell number, and metabolic state. In contrast, aging Abeta(1-42) in the presence of the media supplement B27 inhibited Abeta (1-42) induced neurotoxicity. Differences in the aggregation state of the two preparations did not account for differences in the biological activities elicited by each peptide. Since components of B27 include antioxidants as well as other agents that provide protection against oxidative damage, we suggest that free radicals may be responsible, in part, for the toxicity that occurs following the aging of the peptide.