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Detection of CSF 14-3-3 protein in Guillain–Barré syndrome

From the "Giorgio Spagnol" Service of Clinical Neuroimmunology (A.B., S.A., E.N.-O.), Dino Ferrari Centre, Department of Neurological Sciences, University of Milan, IRCCS Ospedale Maggiore Policlinico (A.B., S.A.), and IRCCS Humanitas Clinical Institute (E.N.-O.), Rozzano, Milan, and Departments of Neurological and Visual Sciences (M.F., G.Z., E.F., M.G., G.S., S.M.) and Science and Technology (H.M.), University of Verona, Italy.

Address correspondence and reprint requests to Dr. S. Monaco, Department of Neurological and Visual Sciences, Section of Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro 10, 37134 Verona, Italy; e-mail: salvatore.monaco{at}univr.it.

Objective: To search for biologic markers in the Guillain–Barré syndrome (GBS), we studied CSF samples from patients with GBS and neuropathy of various etiologies for the presence of 14-3-3 protein.

Methods: CSF samples from patients with GBS, chronic neuropathies, motor neuron disease (MND), definite sporadic Creutzfeldt–Jakob disease (sCJD), and normal control subjects were analyzed by standard immunoblot assay, using a polyclonal anti-14-3-3 antibody. CSF samples were also tested with antibodies recognizing specific isoforms of 14-3-3 proteins, either after one-dimensional or two-dimensional electrophoretic separation.

Results: A positive 14-3-3 assay was observed in 29 of 38 patients with GBS and in 4 patients with MND and other neuropathies, including 2 subjects with vasculitic neuropathy (VN). In GBS, 14-3-3 protein was detected as early as 12 to 48 hours after disease onset and showed an isoform pattern different from that encountered in patients with noninflammatory neuropathies, VN, MND, and sCJD. Immunohistochemical studies performed in archival fatal GBS cases disclosed marked 14-3-3 expression by mononuclear inflammatory infiltrates and Schwann cells.

Conclusion: CSF 14-3-3 assay may represent a useful biologic marker in patients with Guillain–Barré syndrome.

Supported by Associazione Amici Centro Dino Ferrari and by grants from IRCCS Ospedale Maggiore Policlinico, Milan, Italy, NeuroPrion (FOOD-CT-2004-506579), Ricerca Corrente 2004 (IZSLER/04 RC), Ricerca Corrente 2003 (IZSPLVA/03 RC), and the Italian Ministry of Health in collaboration and with the contribution of the Istituto Superiore di Sanità ("Study of pathogenic mechanisms in neurodegenerative disorders for the diagnosis and development of therapeutic approaches") to S. Monaco.

Disclosure: The authors report no conflicts of interest.

Received February 16, 2006. Accepted in final form September 15, 2006.

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