ITSN1 and Alzheimer disease: These data further implicate a role for CME in AD progression given that both the neuronal specific ITSN1-L, and the ubiquitous ITSN1-S, interact with many essential CME proteins (McMahon and Boucrot, 2011; Wong et al., 2012; Gubar et al., 2013; Herrero-Garcia and O'Bryan, 2017), and that overexpression (Sengar, 1999; Simpson et al., 1999) and under-expression (Yu et al., 2008; Thomas et al., 2009) of ITSN1 significantly reduces CME.