A rational approach to treating polyQ diseases is to suppress production of the mutant protein ahead of its deleterious effects. Therefore, silencing the mutant gene would be of therapeutic benefit. Gene silencing therapies have been developed, using either RNA interference (RNAi) or antisense oligonucleotide (ASO) strategies. Both have been proven promising in studies in animal models of polyQ diseases, including SBMA, SCA1, and HD. A number of challenges must be dealt with, however, before these results can be translated to the clinic. The distribution of documents in the CAS Content Collection related to the polyQ disease hallmarks concepts are presented in Figure , while a Sankey graph of the number of documents in which these concepts co-occur with certain disease remedies are shown in Figure . Pathological protein aggregation appears as the most widely discussed attribute of the polyQ diseases, it also co-occurs in documents related to the majority of therapeutic approaches. This is an anticipated observation since protein aggregation is a key pathological hallmark of the majority of neurodegenerative diseases and is in fact related to virtually all other neurodegeneration attributes. Understandably, it most often co-occurs with the aggregation inhibitors as a therapeutic strategy. Chaperone-based therapies also appear as closely targeted to pathological protein aggregation. Neuronal cell death and the aberrant proteostasis are another polyQ disorder attributes discussed along with multiple disease remedies (Figure ). Proteostasis modulators along with the chaperone-based therapies are most frequently targeted to aberrant proteostasis. Neuronal cell death is about equally targeted by several therapeutic strategies: aggregation inhibitors, chaperone-based therapies, and cognitive enhancers. Cognitive enhancers seem like the major strategy towards synaptic and neuronal network dysfunction. Research has revealed that post-translational modifications of the polyglutamine proteins are involved in their neurotoxicity and can significantly modulate it. The distribution of documents in the CAS Content Collection discussing various types of post-translational protein modifications is presented in Figure , and the co-occurrence of these terms with the various members of the polyQ diseases are shown in Figure . Generally, Huntington's disease, which is the subject of the largest number of documents in this subset, co-occurs also with the largest number of documents discussing post-translational modifications. On the other hand, phosphorylation, as the major type of post-translational modification, is related to all kinds of polyQ diseases. The largest part of documents discuss phosphorylation, in association with Huntington's disease. Palmitoylation only co-occurs with Huntington's disease-related documents, while transglutaminationwith Huntington's disease and spinocerebellar ataxias.