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Advances in Psychiatric Treatment (2008) 14: 248-255. doi: 10.1192/apt.bp.106.003319
© 2008 The Royal College of Psychiatrists
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Inflammation and its relevance to psychiatry

Jonathan Cavanagh and Christopher Mathias

Jonathan Cavanagh is a senior lecturer in psychiatry at the University of Glasgow (5th Floor, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, UK. Email: jc199d{at}clinmed.gla.ac.uk) and an honorary consultant psychiatrist to NHS Greater Glasgow & Clyde. He has worked in a variety of clinical and research posts in Edinburgh. His main areas of research are focused on developing neuroimaging measurement in affective disorder in people with medical illnesses. He has a particular interest in the relationship between inflammatory response and brain change in depression in those with medical illnesses. Christopher Mathias is a clinical research fellow working with Dr Cavanagh. On completing house jobs and initial psychiatric training in Edinburgh, he is continuing his psychiatric training in Glasgow. His main research interest is depression in medical illness.

Depression is increasingly recognised as a major public health problem worldwide. The heterogeneity of this condition implies that there may be several neurobiological pathways to depression. This article attempts to explore a pathway that links depression with the inflammatory response. Associations linking inflammation and chronic immune activation with depression have been noted, particularly in the context of (a) medical disorders with inflammatory pathophysiology and (b) immunotherapy for cancer and hepatitis C. Acute coronary syndrome is given as an example of how the inflammatory process might result in depression, and potential mechanisms are discussed. These include: direct action of pro-inflammatory cytokines on the serotonin system, with specific reference to the serotonin transporter; action of cytokines on the hypothalamic–pituitary–adrenal axis; and effects of pro-inflammatory cytokines on neurogenesis in the hippocampus. Reference is made to the potential anti-inflammatory effects of antidepressant drugs and antidepressant effects of anti-inflammatory treatments.








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