We first assessed the effect of miR-22 overexpression in in vitro models of HD comprising lentiviral-mediated expression of mutant Htt fragments (Htt171-82Q versus Htt171-18Q) in primary rat striatal or cortical neurons [15], [16]; these models have previously been shown to exhibit HD-like neuropathologies and gene expression changes [17]. Here, HTT is linked to Huntington disease.