Huntington's disease is an inherited disorder caused by expanded stretch of 
consecutive trinucleotides (cytosine-adenosine-guanine, CAG) within the first 
exon of the huntingtin (HTT) gene on chromosome 4 (p16.3). The mutated 
huntingtin (mHTT) gains toxic function, probably through mechanisms that involve 
aberrant interactions in several pathways, causing cytotoxicity. Pathophysiology 
of disease involves several tissues; indeed it has been shown that there is a 
broad toxic effect of mHTT in the peripheral tissue of patients with HD, not 
only in the central nervous system. In this study we compared gene expression 
profiles (GEP) of HD fibroblasts and matched controls using microarray 
technology. We used RT-PCR to test the consistency of the microarray data and we 
found four genes up-regulated in HD patients with respect to control 
individuals. The genes appear to be involved in different pathways that have 
been shown to be perturbed even in HD models and patients. Although our study is 
preliminary and has to be extended to a larger cohort of HD patients and 
controls, nevertheless it shows that gene expression profiles seem to be altered 
in the fibroblasts of HD patients. Validation of the differential expressions at 
the protein level is required to ascertain if this cell type can be considered a 
suitable model for the identification of HD biomarkers.