For example, the oral administration of trehalose counteracted polyQ toxicity and ameliorated the phenotype, improving motor dysfunction and extended life span in a mouse model of Huntington disease (HD) (43); trehalose administration resulted in a decrease of aggregation of huntingtin mutant protein in several brain areas (but also in liver), thus even when administered orally, it can be adsorbed and a fraction non metabolized in the gastrointestinal tract, can cross the brain blood barrier reaching the neuronal cells affected in HD (43). This evidence concerns the gene HTT and juvenile Huntington disease.