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Axonal damage markers in cerebrospinal fluid are increased in ALS

From the Department of Neurology (J.B., S.D.S., A.C.L., T.H.), University of Ulm, Ulm, Germany; and Department of Neuroinflammation (A.P.), Institute of Neurology, Queen Square, London, UK.

Address correspondence and reprint requests to Dr. Hayrettin Tumani, Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany; e-mail: hayrettin.tumani{at}medizin.uni-ulm.de

Objective: To test whether biomarkers for axonal degeneration correlated with clinical subtypes and were of use in predicting progression of ALS.

Methods: Patients with ALS (n = 69), patients with Alzheimer disease (AD; n = 73), and age-matched controls (n = 33) were included in this prospective study. CSF levels of tau protein and neurofilaments (NfH^SMI35) were measured using ELISA. In 49 patients with ALS, follow-up data were available (median follow-up 7 months).

Results: CSF levels of NfH^SMI35 were five times higher in patients with ALS (1.7 ng/mL) than in controls (0.3 ng/mL, p < 0.001) and 10 times higher than in patients with AD (0.14 ng/mL, p < 0.001). NfH^SMI35 values were also higher in patients with upper motor neuron–dominant ALS than in patients with typical ALS (upper motor neuron + lower motor neuron) at p = 0.02. Values of NfH^SMI35 were higher in ALS of more rapid progression. The values of NfH and tau did not correlate with CSF protein content.

Conclusions: The authors propose that axonal damage markers in CSF may discriminate between subtypes of ALS and that they could be used as markers for therapeutic trials. CSF NfH was superior to tau in these discriminations.

*These authors contributed equally to this work.

Disclosure: The authors report no conflicts of interest.

Received June 28, 2005. Accepted in final form November 30, 2005.

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