Chunk #14 — Introduction — Rationale for the present study: Mechanisms of Alzheimer’s disease identified as upstream regulators of alcohol-sensitive protein networks in C57BL/6J mice
As noted above, a prominent feature of AD neural pathology is the coordinate accumulation of amyloid-β (Aβ) protein (Hardy & Selkoe, 2002) and increased expression or phosphorylation of Tau protein (Ballatore et al., 2007), which promotes plaque and NFT formation, respectively. As part of ongoing work to discover neural mechanisms of alcohol addiction, we assessed the impact of voluntary alcohol intake on the prefrontal cortex (PFC) and amygdala (AMY) proteome in C57BL/6J mice (Agoglia & Hodge, 2017; Salling et al., 2016). These brain regions were chosen for analysis based on known involvement in the rewarding, or reinforcing, effects of alcohol (Agoglia, Holstein, Reid, & Hodge, 2015; Agoglia, Sharko, et al., 2015; Besheer, Cox, & Hodge, 2003; Faccidomo, Reid, Agoglia, Ademola, & Hodge, 2016; Faccidomo, Salling, Galunas, & Hodge, 2015; Hodge, Chappelle, & Samson, 1996; Olive & Hodge, 2000; Salling et al., 2017; Schroeder, Olive, Koenig, & Hodge, 2003; Schroeder et al., 2008; Ueno et al., 2001). In each study, nondependent mice consumed alcohol (10%, v/v) vs water or water only in the home-cage for ~1 month (Fig. 1A). Changes in
