While R6/2 is a well characterized model for studying HD pathogenesisover a short time duration, potential limitations such as fragmentedmutant HTT exon 1 protein overexpression, accelerated disease courseand phenotypic differences from human pathology could affect the translatabilityof results to humans. For example, theneuronal inclusions shown in Figure S53 originate from aggregation of fragmented mutant HTT exon 1 proteins,so the ability of gold NP to deaggregate full-length mutant HTT proteinwill need additional proof. Here, HTT is linked to Huntington disease.