Pharmacologic inhibition of caspases and protein synthesis attenuates cell death induced by Aβ, staurosporine, and Apoptosis Activator II. Neuroneal cultures were treated with 50 μM zVAD-fmk, 10 μg/ml cycloheximide (CHX), or vehicle for 2 h, then exposed to 50 μM Aβ, 0.4 μM staurosporine (STS), 3 μM Apoptosis Activator II (AAII), 25 μM H2O2, 2.5 μM FeCl2/3, 200 nM A23187, 2.5 mM 3-NP, or vehicle for 24 h, and processed for cell viability. Caspase inhibition with zVAD-fmk reduces cell death induced by (a) Aβ, staurosporine, and Apoptosis Activator II, but not (b) H2O2, FeCl2/3, A23187, and 3-NP. Similarly, cycloheximide attenuates neurotoxicity caused by (c) Aβ, staurosporine, and Apoptosis Activator II, but not (d) H2O2, FeCl2/3, A23187, and 3-NP. Data show mean cell viability (± SEM) pooled from 3 independent experiments (n = 3). * P < 0.05 relative to the vehicle-treated control condition.