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

► Pathophysiological Abeta concentrations evoke anti-apoptotic effects. ► AChE-R mediates anti-apoptotic effects via mitochondrial hyperactivity. ► Toxic Abeta concentrations suppress AChE-R expression. ► Cholinergic dynamics (HACU and ChAT adaptation) support AChE-R mediated effects.