As regards the mechanism for melatonin effect on decreasing accumulation of harmful proteins in AD, it has been shown that, in neuronal cells, 0.2−1 μM melatonin binds to death‐associated protein kinase 1 (DAPK1) and dose‐dependently promotes DAPK1 degradation via the ubiquitin‐mediated proteasome pathway, which results in increased activity of Pin1. Here, DAPK1 is linked to Alzheimer disease.