Electrophysiological Correlates of Cognition in Depression

A. Background and Significance Depictions of psychiatric illnesses as stemming largely from biological and genetic vulnerabilities have increased substantially in recent years (Deacon, 2013; Lebowitz & Appelbaum, 2019; Schomerus et al., 2012). These messages are disseminated by physicians, pharmaceutical companies, anti-stigma campaigns, researchers, and the popular media alike. Although at first blush messages emphasizing genetic susceptibility may seem helpful in reducing stigma, growing research points to serious unintended consequences (Haslam & Kvaale, 2015). Specifically, when participants believe their depression is due to biogenetic abnormalities, they expect to suffer for longer periods of time (Kemp, Lickel, & Deacon, 2014), endorse more depressive symptoms (Lebowitz & Ahn, 2017), and feel they have less control over their mood (Lebowitz & Ahn, 2018). Moreover, biogenetic messaging has no impact on stigma (Haslam & Kvaale, 2015). Despite the accumulating self-reported evidence that biogenetic messaging may be harmful, nothing is known about how such messages impact neural correlates of self-reflection and cognitive control - two key processes thought to subserve adaptive self-regulation that may be disrupted among individuals with major depressive disorder (MDD, Pizzagalli, 2011). This study will fill this knowledge gap by comparing resting and task-related electroencephalography (EEG) between adults with MDD randomly assigned to receive either positive or negative information about their genetic susceptibility to depression. Completion of this project will characterize the neural impacts of widespread messages about the etiology of depression. This study may inform clinical decision making, public policy, and guidelines regarding how mental health is discussed.

B. Specific Aims:

Aim1: To examine the impact of biogenetic messaging on default-mode network (DMN) Hypothesis 1: The DMN refers to a network of functionally connected brain regions that are most active at rest and during retrospection (Buckner, Andrews-Hanna, & Schacter, 2008; Raichle, 2015). The DMN has been consistently found to be overactive in the context of depressive disorders (Pizzagalli, 2011), especially in the context of elevated rumination. Capitalizing on approaches to probe DMN functionality using source-localized EEG activity implemented in the mentor's lab (Whitton et al., 2018) the investigators expect that the DMN will be increased following the positive (vulnerable) genetic feedback manipulation. This would indicate that biogenetic messaging increases potentially maladaptive rumination.

Aim 2: To examine the impact of biogenetic messaging on cognitive control Hypothesis 2: Cognitive control refers to a suite of functions that allow humans to monitor, detect, and respond to conflicting information and mistakes, and to mobilize internal resources to resolve such occurrences from happening in the future (Braver, 2012; Miller & Cohen, 2001). One commonly studied facet of cognitive control is error monitoring, which refers to the ability to detect and respond to mistakes. The error-related negativity (ERN) is elicited 0-100ms following an error and the error positivity (Pe) is elicited 200-400ms post-error (Gehring, Liu, Orr, & Carp, 2012). Post-error behavioral adjustments include post-error slowing and post-error improvement in accuracy. Previous research suggests that depressive symptoms correlate with ERN and Pe amplitudes (Compton et al., 2008; Holmes & Pizzagalli, 2008; Olvet, Klein, & Hajcak, 2010; Schroder, Moran, Infantolino, & Moser, 2013). Induction of genetic messaging about intelligence increased the Pe amplitude but also reduced the correlation between Pe and post-error performance (Schroder, Moran, Donnellan, & Moser, 2014). Accordingly, in the current study, the investigators expect the Pe to be increased and a reduced relationship between Pe and post-error behavior in the vulnerable genetic condition.

Aim 3: To evaluate self-reported motivation for treatment, expectancies, and preferences Hypothesis 3: Previous research has documented a cost in self-reported motivation and future expectancies following receiving biogenetic information about depression (Kemp et al., 2014; Lebowitz & Ahn, 2017). The investigators expect to replicate these effects in a sample of individuals with MDD. The investigators expect that participants receiving vulnerable genetic feedback will 1) endorse poorer perceived control over their emotions, 2) expect to have depression for a longer period of time, 3) endorse a preference for pharmacotherapy versus psychotherapy and 4) view pharmacotherapy as more effective than psychotherapy.