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Nexo B.A.,University of Aarhus | Christensen T.,University of Aarhus | Frederiksen J.,Glostrup Hospital | Moller-Larsen A.,University of Aarhus | And 24 more authors.
PLoS ONE | Year: 2011

We have investigated the role of human endogenous retroviruses in multiple sclerosis by analyzing the DNA of patients and controls in 4 cohorts for associations between multiple sclerosis and polymorphisms near viral restriction genes or near endogenous retroviral loci with one or more intact or almost-intact genes. We found that SNPs in the gene TRIM5 were inversely correlated with disease. Conversely, SNPs around one retroviral locus, HERV-Fc1, showed a highly significant association with disease. The latter association was limited to a narrow region that contains no other known genes. We conclude that HERV-Fc1 and TRIM5 play a role in the etiology of multiple sclerosis. If these results are confirmed, they point to new modes of treatment for multiple sclerosis. © 2011 Nexø et al.

Bukh J.D.,Copenhagen University | Bock C.,Copenhagen University | Vinberg M.,Copenhagen University | Werge T.,Research Institute of Biological Psychiatry | And 2 more authors.
European Neuropsychopharmacology | Year: 2010

Genetic polymorphisms seem to influence the response on antidepressant treatment and moderate the impact of stress on depression. The present study aimed to assess, whether allelic variants and stressful life events interact on the clinical outcome of depression. In a sample of 290 systematically recruited patients diagnosed with a single depressive episode according to ICD-10, we assessed the outcome of antidepressant treatment and the presence of stressful life events in a 6-month period preceding onset of depression by means of structured interviews. Further, we genotyped nine polymorphisms in the genes encoding the serotonin transporter, brain derived neurotrophic factor, catechol-. O-methyltransferase, angiotensin converting enzyme, tryptophan hydroxylase, and the serotonin receptors 1A, 2A, and 2C. We found no evidence that the effects of the genetic polymorphisms on treatment outcome were dependent on stressful life events experienced by the individual prior to onset of depression. © 2009 Elsevier B.V. and ECNP.

Haastrup E.,Copenhagen University | Bukh J.D.,Copenhagen University | Bock C.,Copenhagen University | Vinberg M.,Copenhagen University | And 5 more authors.
Journal of Affective Disorders | Year: 2012

Background: Depression is accompanied by an inflammatory reaction and activation of cell mediated immunity (CMI) and stressors may induce the cytokine network in humans. The proinflammatory cytokine interleukin-18 (IL-18) is less investigated in depression but highly relevant since it is produced by activated macrophages and expressed in the brain. Methods: The distribution of six polymorphisms in IL10, IL18 and NF was compared between patients with a single episode of depression either preceded by a stressful life event (n = 182), or occurring without a prior stressful life event (n = 106) and a group of healthy control individuals (n = 335). Results: The major C allele of the IL18 rs187238 and the major G allele of rs1946518 had a significantly higher prevalence among the patients with a stressful life event prior to onset of disease than both patients without a stressful life event and compared with the healthy controls individuals. None of the examined IL10 or NF alleles were differently distributed among these groups. Limitations: Data are nominally significant and not resistant to correction for multiple testing. Conclusion: The major C allele of the IL18 rs187238 and the major G allele rs1946518 have previously been associated with higher expression of IL-18 mRNA. Our data suggest that this genetic trend towards higher IL-18 production may increase the susceptibility to depression in response to stressful life events. © 2011 Elsevier B.V.

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