Evidence for an Inflammatory Subtype of Adult Depression

• In Event: 1-015 - Translational Perspectives on the Role of Inflammation in Brain Development and Function

Integrative Statement

There is growing evidence to suggest that chronic inflammation may contribute to transdiagnostic symptoms of low motivation, apathy and anhedonia. Specifically, data from human and animal models suggest that increased inflammatory cytokines may disrupt dopamine synthesis and synaptic availability within critical corticostriatal reward circuitry, including the ventral striatum and ventromedial prefrontal cortex (vmPFC). In this presentation, I will first present data from a recent neuroimaging study of 65 healthy female participants revealing a novel link between stress-induced inflammation and reward activity in the ventral striatum. Specifically, we show that acute stress exposure increased levels of the inflammatory cytokine interleukin-6 (IL-6) (F(1.43,92) = 17.89, p = 0.000008, partial eta2 = 0.28), and that individual differences in the magnitude of stress-induced IL-6 predicted stress-induced decreases in reward prediction error BOLD signals in the ventral striatum (r = -0.54, p < 0.05; see figure 1). Next, I will present interim analyses from a placebo-controlled clinical trial in which depressed patients with elevated inflammation (C-reactive protein > 3.0 mg/l) are treated with the potent TNF-alpha antagonist inflixmab. Data from pre/post neuroimaging tasks assessing reward anticipation and motivation will be presented. Taken together, these studies extend prior empirical and theoretical work positing that increased risk for depression following stress may partly result from effects of stress-induced immunoreactivity on basal-ganglia function.

Author

• Michael T Treadway, Emory University
  Presenting Author