Despite some classical studies showed that both KA and IA produced degeneration of striatal neurons, as well as reduction of glutamate decarboxylase (GAD) and choline acetyltransferase (CAT) activities – two hallmarks of HD - in animal models [211,212], these plant-derived agents were simply unable to mimic other specific morphological and neurochemical features of HD. The gene discussed is GAD1; the disease is Huntington disease.