PROINFLAMMATORY AND “RESILIENCY” PROTEINS IN THE CSF OF PATIENTS WITH MAJOR DEPRESSION
Article first published online: 2 SEP 2011
© 2011 Wiley-Liss, Inc.
Depression and Anxiety
Volume 29, Issue 1, pages 32–38, January 2012
How to Cite
Martinez, J. M., Garakani, A., Yehuda, R. and Gorman, J. M. (2012), PROINFLAMMATORY AND “RESILIENCY” PROTEINS IN THE CSF OF PATIENTS WITH MAJOR DEPRESSION. Depress. Anxiety, 29: 32–38. doi: 10.1002/da.20876
- Issue published online: 23 JAN 2012
- Article first published online: 2 SEP 2011
- Manuscript Accepted: 5 JUL 2011
- Manuscript Revised: 28 JUN 2011
- Manuscript Received: 29 JAN 2011
- National Institutes of Health (NIH). Grant Numbers: R01-MH58808, K08-MH6701
- brain-derived neurotrophic factor;
- cerebrospinal fluid;
- neuropeptide Y;
A number of studies have shown that elevated levels of inflammatory cytokines may promote depression and suicidal ideation and that neuroprotective peptides may decrease the response to stress and depression. In this study, cerebrospinal fluid (CSF) levels of three inflammatory cytokines (IL-1, IL-6, and tumor necrosis factor α (TNFα)) and two putative “resiliency” neuropeptides (brain-derived neurotrophic factor (BDNF) and neuropeptide Y (NPY)) were compared between patients with depression and healthy controls.
Eighteen patients with major depression and 25 healthy controls underwent a lumbar puncture; CSF samples were withdrawn and assayed for IL-1, IL-6, TNFα, BDNF, and NPY levels. Patients with depression were then entered into an 8-week treatment protocol and had repeated lumbar puncture procedures post-treatment.
Contrary to prediction, we found that at baseline depressed patients had higher CSF NPY concentration compared to the normal comparison group. Within the depressed patients, we found several statistically significant correlations between elevated CSF cytokine levels and clinical severity.
Despite the small sample size, given the challenges in obtaining CSF from patients with depression these data are of interest in confirming some aspects of the inflammatory hypothesis of depression.