Mutations in the HTT gene, consisting of expansion of CAG triplets, cause the 
Huntington's disease (HD), one of the major neurodegenerative disorders. 
Formation of aggregates of mutant huntingtin (mHTT, the product of the mutant 
HTT gene) leads to cellular dysfunctions, and subsequent neurodegeneration which 
manifest clinically as motor abnormalities and cognitive deficits. We recently 
used immortalized HEK-293 cells expressing the 1st exon of the mutant HTT gene 
as a cellular model of HD, and showed that the stimulation of autophagy by 
genistein corrected the mutant phenotype. However, effects of genistein on HD 
patient-derived cells remained unknown. In this report, we demonstrated that 
genistein also instigated degradation of mHTT in fibroblasts derived from HD 
patients. This was assessed as a significant decrease in the levels of HTT in HD 
fibroblasts measured by Western-blotting, and the disappearance of intracellular 
mHTT aggregates in cells observed by fluorescent microscopy. Fibroblasts derived 
from control persons were not affected by genistein treatment. These results 
indicate that genistein can improve HD phenotype in patient-derived cells, and 
substantiates the need for further studies of this isoflavone as a potential 
therapeutic agent.