Our aim:

Contribute to the understanding of psychobiological vulnerability to depression.

What we know:

• Cognitive models of depression suggest that biased emotion processing, favoring the processing of negative emotional stimuli, underlies the onset and maintenance of depression.
• Behavioral studies demonstrated a negative bias in attention, interpretation, and memory in patients with acute depression. These cognitive biases were found to operate even in early, automatic (subliminal) stages of processing.
• A negative bias in emotion processing has been associated with future depressive relapses.
• Cross-sectional neuroimaging studies provided evidence for brain functional alterations already in the early, automatic stages, mainly in the amygdala, a key region of the emotion processing and salience network: Patients in acute depression show amygdala hyperactivity to subliminally presented negative stimuli.

Our key question:

Is this abnormality in automatic negative processing an enduring neurofunctional “trait” of depression or is it rather associated with the depressive "state" itself?

Our methods:

We measured brain function in acutely depressed patients and healthy subjects with fMRI during an affective priming task in which emotional faces were presented (subliminally) for a brief moment. We then repeated this investigation after two years.

Our main findings:

During automatic emotion processing, healthy controls show higher amygdala activity to happy compared to sad faces. In acute depression, this pattern seems to be reversed: Patients show amygdala hyperactivity to sad faces and comparatively lower amygdala activity to happy faces.

But does this bias change in remission of depression?

After two years, all patients still showed amygdala hyperactivity to subliminally presented sad faces, even the patients who were remitted from depression.

Our conclusion:

Our study indicates that automatic amygdala hyperactivity to negative stimuli persists even when patients are remitted from depression. This could be interpreted as an enduring trait marker of depression, possibly representing a neural correlate of vulnerability to or a consequence of depression.