These data suggest two possible scenarios: either the increased interaction of AMPK-α1 with the SIRT1-DBC1 complex might attempt to promote SIRT1 activation in the striatum of HD mice through the dissociation from DBC1, or the inability to induce SIRT1 in R6/2 mice might be due to an inhibitory retention of AMPK-α1 via DBC1. This evidence concerns the gene SIRT1 and Huntington disease.