The conditions under which beta-amyloid (A beta) is toxic to primary r
at hippocampal neurons were investigated. Synthetic A beta(1-42) pepti
de was neurotoxic following ''aging'' for 7 to 14 days at 37 degrees C
in modified Eagle's media. Neurotoxicity included decreases in neurit
e length, cell number, and metabolic state. In contrast, aging A beta(
1-42) in the presence of the media supplement B27 inhibited A beta(1-4
2)-induced neurotoxicity. Differences in the aggregation state of the
two preparations did not account for differences in the biological act
ivities elicited by each peptide. Since components of B27 include anti
oxidants as well as other agents that provide protection against oxida
tive damage, we suggest that free radicals may be responsible, in part
, for the toxicity that occurs following the aging of the peptide. (C)
1996 Academic Press, Inc.