Alterations in the catalytic activity of ChAT have been observed in several protein misfolding neurological diseases, including AD and Huntington's disease (Lange et al., 1992; Pakaski and Kalman, 2008), both of which are known to exhibit dysfunction of HSPs and other molecular chaperones, accumulation of aggregate-prone proteins, and build-up of proteotoxic and oxidative stress (Mati et al., 2014; Lackie et al., 2017). Here, CHAT is linked to juvenile Huntington disease.