Connectivity between lateral frontal, dorsal cingulate, and dorsal parietal cortices appears to be critical for many components of executive cognition, as it is consistently observed during tasks that index working memory, goal-directed attention, conflict detection,

and online performance monitoring (Dosenbach et al., 2007, Wang et al., 2010b, Cole and Schneider, 2007, Stevens et al., 2009 and Hampson et al., 2006). Deficits in executive cognition comprise a symptom domain that spans a number of disorders, including schizophrenia, attention-deficit/hyperactivity disorder (ADHD), major depressive disorder (MDD), and substance abuse (Barkley, 1997, Garavan and Hester, 2007, Barch and Smith, 2008, Luck and Gold, 2008 and Murrough www.selleckchem.com/products/ABT-263.html et al., 2011). Common patterns of atypical connectivity within a dorsal lateral prefrontal-cingulate-parietal

network are apparent across these disorders, and may contribute to symptoms relating to attention, working memory, and cognitive control (Tan et al., 2006, Schlösser et al., 2008, Vasic et al., 2009, Woodward et al., 2009, Castellanos and Proal, 2012 and Ma et al., 2010). This is consistent with the idea that the common expression of cognitive symptoms among categorically distinct psychopathologies arises from common network pathology. The amygdala, medial prefrontal cortex (ventromedial and medial orbital aspects, along with perigenual cingulate cortex) and lateral prefrontal cortex comprise a corticolimbic circuit that is important for engendering and regulating vigilance and arousal responses to

biologically salient stimuli (Pessoa, 2010 and Kim PLX4032 et al., 2011). This circuit is consistently engaged during tasks that evoke negative emotional arousal or require the regulation of negative emotional responses (Zald, 2003), suggesting involvement in aversive affective experiences. Affective symptoms such as anxiety, anger, rumination, and hypervigilance are common to many forms of psychopathology, being especially prominent in mood, anxiety and personality disorders. Similar patterns of corticolimbic circuit dysfunction cut across diagnostic taxons, and may explain the transdiagnostic nature of negative affect symptoms. For example, cingulate-amygdala through circuit dysfunction predicts high levels of trait negative affect (Pezawas et al., 2005 and Cremers et al., 2010), and is evident in schizophrenia (Rasetti et al., 2009), conduct disorder (Marsh et al., 2008), and substance dependence (Upadhyay et al., 2010) in addition to mood and anxiety disorders (Matthews et al., 2008, Dannlowski et al., 2009, Etkin et al., 2010, Etkin and Schatzberg, 2011 and Lui et al., 2011). Of note, cross-diagnostic analyses confirm that cingulate-amygdala dysconnectivity is a source of common affective vulnerability in generalized anxiety disorder and MDD (Etkin and Schatzberg, 2011).