To detect ncRNAs involved in the pathogenesis of HD, one study examined the ncRNA expression profile of human HD brain tissue and found that the expression of the lncRNAs HAR1F and HAR1R, which are antisense transcripts of the first human accelerated region 1 (HAR1) gene, was significantly reduced in the striatum. These lncRNAs are involved in neurotransmission, memory structure, and synaptic plasticity in the mature brain, and their aberrant expression is also associated with HD.41 The same study also demonstrated that abnormal REST nuclear-cytoplasmic exchange in the striatum of HD led to effective transcriptional repression of HAR1.42 The lncRNA DGCR5 is a transcript of DiGeorge critical region 5 (DGCR5) and includes a genome-binding site for REST, which plays an important transcriptional regulatory role in HD.43 The expression of the lncRNA MEG3, encoded by maternally expressed gene 3 (MEG3), was downregulated in HD brain tissue, and its downregulation was also inhibited by REST.44 There is much disparate research showing that MEG3 may be an important epigenetic regulator in the developing and adult human brain, which may stably alter gene expression in response to neuronal activity. If so, the downregulation of MEG3 in HD could plausibly have serious consequences. Overexpression of the lncRNA Abhd11os (ABHD11-AS1 in humans) attenuates the toxicity of Htt mRNA in murine models of HD. Studies have shown that knocking out the Abhd11os gene in the HD mouse model produces neurotoxicity, whereas overexpression of Abhd11os has a neuroprotective effect.45