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Tau protein level in cerebrospinal fluid is increased in patients with early multiple sclerosis

Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany

M Maier

Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany

S Arda

Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany

A Claus

Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany

S D Süssmuth

Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany

J Kassubek

Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany

H Tumani

Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany, hayrettin.tumani{at}medizin.uni-ulm.de

Axonal damage has been proposed as the major substrate of permanent clinical disability in multiple sclerosis. Tau protein, a microtubule-associated protein localised in neuronal axons, may serve as a biochemical surrogate marker to evaluate axonal damage in vivo.We intended to determine the extent of axonal damage in different stages and clinical subtypes of MS by investigating cerebrospinal fluid tau concentrations. Tau was measured using an immunoassay in 35 patients with relapsing—remitting MS, eight patients with secondary progressive MS, nine patients with primary progressive MS, 50 patients with clinically isolated syndrome suggestive of early MS and 46 normal controls. Cerebrospinal fluid tau was significantly elevated in MS compared with normal controls (median 206.0 pg/mL versus152.0 pg/mL;P=0.002). No significant difference among different subtypes of MS could be detected, although highest levels were found in very early disease stages. There was a significant elevation of CSF tau among patients with gadolinium-enhancing brain lesions in magnetic resonance imaging (P=0.02) and a tendency towards higher CSF tau levels in patients with pronounced intrathecal IgG synthesis, supporting the notion that axonal damage is influenced by inflammatory activity.

Key Words: axonal damage • cerebrospinal fluid • clinically isolated syndrome • multiple sclerosis • relapse-remitting • tau protein

Multiple Sclerosis, Vol. 11, No. 3, 261-265 (2005)
DOI: 10.1191/1352458505ms1159oa


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