Moreover, the co-localization of SQSTM1/p62 and Keap-1 insoluble deposits was observed in AD brain extracts [98], and the impairment to the promoter of SQSTM1/p62 as well as co-localization of SQSTM1/p62 with protein aggregation have been observed in other neuropathies, such as Huntington’s disease, tauopathy, and α-synucleinopathies [94,96]. This evidence concerns the gene SQSTM1 and juvenile Huntington disease.