Pathophysiological amyloid concentrations induce sustained upregulation of readthrough acetylcholinesterase mediating anti-apoptotic effects.

Cholinergically differentiated SH-SY5Y neuroblastoma cells were treated with a pathophysiologically relevant, low (300 nM), and a high (3 μM) dose of amyloid beta 1-42 (Abeta) or 42-1 (revAbeta). At early (1 and 4h) and late (24h) time points, the pro- and anti-apoptotic factors--caspase-3 and p53, and B-cell lymphoma 2 protein (Bcl-2), respectively--were… CONTINUE READING