While the current study only assessed female BAC HD animals, food restriction performed in the HD-N171-82Q mouse model of HD, which express human N-terminal truncated huntingtin with 82 polyglutamine repeats driven by the mouse prion promoter 26, also resulted in a delay in the onset of motor deficits as well as a normalization of glucose metabolism and brain BDNF levels 27. The gene discussed is HTT; the disease is Huntington disease.