IFNB1 and juvenile Huntington disease: GSEA of Ifnb+/+ and Ifnb–/– showed enrichment of genes associated with Huntington’s disease (HD), PD, AD, and prion diseases, and rIFN-β caused the Ifnb–/– profile to resemble WT (Figure 2J), supporting that common pathways link neurodegenerative diseases (Shulman and De Jager, 2009).