Enhanced cytotoxicity of amyloid beta-peptide by a complement dependent mechanism.
Amyloid beta-peptide (A beta) has been shown to activate the classical complement pathway in vitro. Here, we demonstrate that this interaction is fully capable of killing cells and damaging cellular processes in mixed hippocampal cultures from embryonic day 18 rat fetuses. Lactic acid dehydrogenase (LDH) release and morphologic changes were used to evaluate toxicity.
L.J. Roberts Center, Sun Health Research Institute, Sun City, AZ 85372.
J
J
Schultz
J
J
Schaller
M
M
McKinley
B
B
Bradt
N
N
Cooper
P
P
May
J
J
Rogers
D016564:Amyloid beta-Protein Precursor / Q000633:toxicity*; D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D003171:Complement Pathway, Classical / Q000187:drug effects / Q000502:physiology*; D003165:Complement System Proteins / Q000502:physiology*; D004622:Embryo, Mammalian; D005260:Female; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects*; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000473:pathology; D009498:Neurotoxins / Q000633:toxicity; D009924:Organ Culture Techniques; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley
D016564:Amyloid beta-Protein Precursor; D009498:Neurotoxins; D003165:Complement System Proteins; D007770:L-Lactate Dehydrogenase