“…It is already known that the source of FRN is located in the ACC (Holroyd and Coles, 2002; Hajcak et al, 2007; Bellebaum and Daum, 2008; Holroyd et al, 2009), and abnormalities of the ACC in AD have been reported at histopathological and physiological levels. In AD patients, accumulation of both beta amyloid and tau (Morishima-Kawashima and Ihara, 2002; Leuba et al, 2009; Murphy and LeVine, 2010; Bloom, 2014), metabolic changes (Bracco et al, 2007; Lim et al, 2012), and decreased blood flows (Dukart et al, 2013; Long et al, 2013; Terada et al, 2013; Lin et al, 2014; Bailly et al, 2015) are observed in the ACC. The ACC is atrophied structurally (Buckner et al, 2005; Jones et al, 2006; Seeley et al, 2009; Krueger et al, 2010), and the anatomical connectivity with other areas is also impaired (Greicius et al, 2004; Rombouts et al, 2005; Wang et al, 2007; Boublay et al, 2016; Hafkemeijer et al, 2016b).…”