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Inflammation causes mood changes through alterations in subgenual cingulate activity and mesolimbic connectivity.
Neil A Harrison1, Lena Brydon, Cicely Walker
1Wellcome Trust, Centre for Neuroimaging, Institute of Cognitive Neuroscience, UCL, 17 Queen Square, London WC1N 3AR, UK. n.harrison@fil.ion.ucl.ac.uk
Biological Psychiatry
|May 9, 2009
Summary
Inflammation significantly reduces mood by altering brain activity in regions like the subgenual anterior cingulate cortex (sACC). This mood change is linked to reduced sACC connectivity, suggesting a common pathway for depression and sickness-associated mood changes.
Area of Science:
- Neuroscience
- Psychiatry
- Immunology
Background:
- Inflammatory cytokines are linked to depression pathophysiology.
- Systemic inflammatory cytokines induce depression-like behaviors in rodents and clinical depression in humans.
- Elevated pro-inflammatory cytokines are observed in patients with depression.
Purpose of the Study:
- To investigate the neural mechanisms of inflammation-associated mood changes.
- To examine the modulatory effects of inflammation on mood regulation circuits.
- To understand the neurobiological correlates of mood changes during inflammation.
Main Methods:
- A double-blind, randomized crossover study involving 16 healthy male volunteers.
- Participants received typhoid vaccination or placebo, with mood assessed via questionnaires.
- Functional magnetic resonance imaging (fMRI) was used during an emotional face perception task.
Main Results:
- Typhoid vaccination induced an inflammatory response (increased interleukin-6) and mood reduction.
- Mood deterioration correlated with increased subgenual anterior cingulate cortex (sACC) activity during emotional processing.
- Inflammation reduced sACC connectivity to key brain regions, modulated by interleukin-6.
Conclusions:
- Inflammation-associated mood changes involve alterations in sACC activity and functional connectivity.
- Peripheral cytokines influence mood-dependent sACC connectivity.
- Suggests a shared pathophysiological basis for major depressive disorder and sickness-associated mood changes.
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