Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/19661
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dc.contributor.authorTsakiri, A.-
dc.contributor.authorRAVANIDIS, Stelios-
dc.contributor.authorLagoudaki, R.-
dc.contributor.authorPoulatsidou, K.N.-
dc.contributor.authorSvane, I.M.-
dc.contributor.authorFrederiksen, J.L.-
dc.contributor.authorGrigoriadis, N.-
dc.date.accessioned2015-10-05T13:51:29Z-
dc.date.available2015-10-05T13:51:29Z-
dc.date.issued2015-
dc.identifier.citationACTA NEUROLOGICA SCANDINAVICA, 131 (5), p. 305-312-
dc.identifier.issn0001-6314-
dc.identifier.urihttp://hdl.handle.net/1942/19661-
dc.description.abstractObjective The aim of the study was to investigate the expression of different immunological mediators in blood and CSF in patients with acute ON and to estimate whether they were implicated in pro- or anti-inflammatory or even regulatory reactions in comparison with a healthy control group (HC). Methods Sixty-four patients between 18 and 59 years of age suffering by acute ON, onset of <4 weeks, were included in the study. Visual tests and brain magnetic resonance imaging (MRI) were performed in ON. Blood and CSF samples were collected from untreated patients and from a gender- and age-matched voluntary HC (n = 32). The mRNA expression of distinct cytokines and neurotrophic factors was assessed by semi/quantitative real-time PCR (RT-PCR). Results Brain- and glial cell-derived neurotrophic factor (BDNF and GDNF) and interleukin 10 (IL-10) expression was significantly increased in the CSF compared to the blood in both ON and HC (P < 0.001). In the CSF increased levels of BDNF and GDNF of the ON group were positively correlated with the presence of oligoclonal bands (OB). Additionally, patients with gadolinium (gd+) lesions on brain MRI showed increased levels of IL-5 in blood (P = 0.03). Conclusion Our data indicate that both immuno-regulatory and neuroprotective mechanisms may potentially take place relatively early in the course of the ON. The presence of neurotrophic factors in healthy CSF and their overexpression already during the acute phase of ON supports the alertness of CNS defence mechanisms ready to be activated during degenerative events, such as destruction of the myelin.-
dc.description.sponsorshipWe would like to thank the molecular biologist Dimitrios Tsiantoulas, AHEPA University Hospital, Thessaloniki Greece for his supervision and the contribution to the design of primer's sequence. We thank the statistician of the study Judith Jacobsen, StatconApS Denmark, for the statistical analysis. We are also grateful to Matilda Degn Vinther human biologist, PhD, Glostrup Research Institute, Denmark, for her helpful comments to the present work. The study was supported by private Funds: Dir. Jacob Madsen & hustru Olga Madsens Fond, Civilingenioer Bent BoeghoghustruIngeBoehs Fond, and A.P. Moeller oghustru-Chastine Mc-Kinney Moellers Fond.-
dc.language.isoen-
dc.rights© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd-
dc.subject.othercytokines; FOXP3; multiple sclerosis; optic neuritis; neurotrophic factors-
dc.titleNeuroprotective and anti-inflammatory mechanisms are activated early in Optic Neuritis-
dc.typeJournal Contribution-
dc.identifier.epage312-
dc.identifier.issue5-
dc.identifier.spage305-
dc.identifier.volume131-
local.bibliographicCitation.jcatA1-
local.type.refereedRefereed-
local.type.specifiedArticle-
dc.identifier.doi10.1111/ane.12344-
dc.identifier.isi000352526300007-
item.accessRightsRestricted Access-
item.fulltextWith Fulltext-
item.fullcitationTsakiri, A.; RAVANIDIS, Stelios; Lagoudaki, R.; Poulatsidou, K.N.; Svane, I.M.; Frederiksen, J.L. & Grigoriadis, N. (2015) Neuroprotective and anti-inflammatory mechanisms are activated early in Optic Neuritis. In: ACTA NEUROLOGICA SCANDINAVICA, 131 (5), p. 305-312.-
item.contributorTsakiri, A.-
item.contributorRAVANIDIS, Stelios-
item.contributorLagoudaki, R.-
item.contributorPoulatsidou, K.N.-
item.contributorSvane, I.M.-
item.contributorFrederiksen, J.L.-
item.contributorGrigoriadis, N.-
item.validationecoom 2016-
crisitem.journal.issn0001-6314-
crisitem.journal.eissn1600-0404-
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