Prevention of Amyloid-Beta Oligomer-Induced Neuronal Death by EGTA, Estradiol, and Endocytosis Inhibitor
Abstract
Material and Methods. Primary cultures of CGC were treated with various aggregate forms of Aβ1–42. Cell viability was assessed by fluorescent microscopy using propidium iodide and Hoechst 33342 staining.
Results. Exposure of neurons to 500 nM Aβ1–42 oligomers for 72–168 h caused extensive neuronal necrosis. Lower concentrations (100–250 nM) were not toxic to cells during 7 days of incubation. Aβ1–42 monomers and fibrils had no effect on neuronal viability even after 7 days of incubation. Treatment of neurons with EGTA, steroid hormone 17β-estradiol, and methyl-β-cyclodextrin significantly reduced Aβ1-42 oligomers-induced neuronal death.
Conclusions. The results show that submicromolar concentrations of Aβ1-42 oligomers were highly toxic to neurons during protracted incubation inducing neuronal necrosis that can be prevented by chelating extracellular Ca2+ with EGTA, inhibiting endocytosis with methyl-β-cyclodextrin, or by estradiol, which may protect against mitochondrial permeability transition pore opening.
Share and Cite
Čižas, P.; Jekabsonė, A.; Borutaitė, V.; Morkūnienė, R. Prevention of Amyloid-Beta Oligomer-Induced Neuronal Death by EGTA, Estradiol, and Endocytosis Inhibitor. Medicina 2011, 47, 15. https://doi.org/10.3390/medicina47020015
Čižas P, Jekabsonė A, Borutaitė V, Morkūnienė R. Prevention of Amyloid-Beta Oligomer-Induced Neuronal Death by EGTA, Estradiol, and Endocytosis Inhibitor. Medicina. 2011; 47(2):15. https://doi.org/10.3390/medicina47020015
Chicago/Turabian StyleČižas, Paulius, Aistė Jekabsonė, Vilmantė Borutaitė, and Ramunė Morkūnienė. 2011. "Prevention of Amyloid-Beta Oligomer-Induced Neuronal Death by EGTA, Estradiol, and Endocytosis Inhibitor" Medicina 47, no. 2: 15. https://doi.org/10.3390/medicina47020015