IntroductionTau protein is a potential marker of neuronal damage. The aim of the study is to investigate its potential role as a marker of brain atrophy in multiple sclerosis (MS).Materials and methodsCerebrospinal fluid (CSF) and blood samples were collected from 48 patients with multiple sclerosis. Total-tau (t-tau) and phospho181Thr-tau (p-tau) concentrations were assayed with commercially available INNOTEST® hTAU Ag and INNOTEST® phospho181Thr-tau(181P) and correlated with indices of brain atrophy in magnetic resonance imaging (MRI) and clinical characteristics of the study population.ResultsT-tau concentration in CSF was significantly higher in relapsing-remitting (RR) compared to secondary progressive (SP) MS patients (P = 0.01). Brain parenchymal fraction (BPF) was significantly decreased in SP patients (P = 0.002). BPF in the whole study population correlated inversely with Expanded Disability Status Scale (EDSS) (r = –0.51, P = 0.0002) and Multiple Sclerosis Severity Score (MSSS) (r = –0.42, P = 0.002). T-tau in CSF in the whole patient group correlated inversely with EDSS (r = –0.58, P = 0.0006).ConclusionsThe results of our study suggest that total-tau concentration in CSF in a MS population decreases in the course of disease and reflects degree of parenchymal brain loss.
BACKGROUND AND PURPOSE: Spectroscopic studies (1 H-MR spectroscopy) of normal-appearing white matter (NAWM) in patients with multiple sclerosis (MS) with MR imaging brain lesions have already been performed, but our intention was to investigate NAWM in MS patients who lack brain lesions to elucidate whether the same pathologic changes could be identified.
CSF levels of tTau and S100b are elevated in patients with MS and can reflect an axonal and glial pathology. Measurement of serum concentrations of S100b may be useful for monitoring immunosuppressive therapy and may support clinical assessment. In contrast, tTau concentration did not prove to be a useful marker of mitoxantrone therapy.
AbstractIn search of biological marker in multiple sclerosis (MS), total-tau and phospho-tau (Thr181) concentrations were established in CSF and serum of 78 patients with MS, using commercially available kits. Serum and CSF concentrations of IgG, IgM, and albumin were assayed simultaneously to calculate quotients and indices of intrathecal synthesis. Serum t-tau detection was strikingly low (23.1%); therefore, this factor was excluded from further analysis. Serum p-tau levels did not correlate with any of indices or quotients. Unexpectedly, CSF t-tau and p-tau showed an inverse relation with MSSS and EDSS, which has not been published elsewhere. Our results do not support utility of serum t-tau and p-tau as surrogate markers for MS.
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