Dysfunction of the TGF-β signaling in the brains of AD patients and in mouse models of AD may accelerate Aβ deposition and neurodegeneration (Tesseur et al., 2006) and silencing a subset of TGF-β signaling would promote adverse effects of AD in transgenic C. elegans including deposition of β-amyloid (Haque and Nazir, 2016). This evidence concerns the gene TGFB1 and Alzheimer disease.