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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/19661

Title: Neuroprotective and anti-inflammatory mechanisms are activated early in Optic Neuritis
Authors: Tsakiri, A.
Ravanidis, Stelios
Lagoudaki, R.
Poulatsidou, K.N.
Svane, I.M.
Frederiksen, J.L.
Grigoriadis, N.
Issue Date: 2015
Citation: ACTA NEUROLOGICA SCANDINAVICA, 131 (5), p. 305-312
Abstract: Objective 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.
URI: http://hdl.handle.net/1942/19661
DOI: 10.1111/ane.12344
ISI #: 000352526300007
ISSN: 0001-6314
Category: A1
Type: Journal Contribution
Validation: ecoom, 2016
Appears in Collections: Research publications

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