In the present study, we show that IDN5706 disrupts APP glycosylation (Fig 7B), and stimulates the degradation of iAPP through Atg5-dependent autophagy (Figs 8 and 9), with a resulting reduction in the processing of APP to CTFs, which could have beneficial effects to Alzheimer's disease. The gene discussed is ATG5; the disease is early-onset autosomal dominant Alzheimer disease.