Cultured neurons treated with low doses of annonacin exhibit hallmarks of tauopathy, including increased tau concentration, tau hyperphosphorylation, cell death and somatodendritic redistribution of hyperphosphorylated tau in a manner dependent on mitochondrial complex I activity (Lannuzel et al, 2003; Escobar‐Khondiker et al, 2007; Yamada et al, 2014). This evidence concerns the gene MAPT and tauopathy.