Affiliation: | (1) Dept. of Neurology, Medical University, Jaczewskiego 8, 20-090 Lublin, Poland;(2) Dept. of Neurology, Karl-Franzens University, Graz, Austria |
Abstract: | Abstract. Recently it has been shown that axonal damage occurs inall stages of multiple sclerosis (MS) and can be detected veryearly in the course of the disease. Axonal pathology has beenrelated to the inflammatory demyelinating environment, but itsdependence on inflammation is still unknown. We measured tauprotein and 14-3-3, two intracellular proteins expressed inneurons and glial cells, in the cerebrospinal fluid (CSF) of 114patients with MS, in 79 patients with other inflammatoryneurological diseases (IND) and in the CSF of 60 patients withnon-inflammatory neurological diseases (NIND) as controls.Concentrations of tau protein and 14-3-3 were measured byenzymelinked immunoassay and were correlated to the followingimmune parameters in the CSF: leukocyte cell count, totalprotein, albumin CSF/serum ratio as a marker of disruption ofthe blood-brain barrier, immunoglobulin (IgG concentrations andIgG index as an indicator for intrathecal synthesis of IgG inthe CSF). Both in MS and IND tau protein levels weresignificantly higher than in NIND (p < 0.05). In MS patientslevels of tau protein were positively correlated with the IgGindex (p < 0.05) and this association was present in bothrelapsing remitting MS (RRMS) (p < 0.05) and progressive MS(p < 0.05). Tau and 14-3-3 were also correlated with the IgGindex in patients with IND (p < 0.05). These findingsstrengthen the hypothesis that inflammation may be at least inpart responsible for the axonal damage observed in MSpatients. |