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More MS news articles for May 2003

A new paraclinical CSF marker for hypoxia-like tissue damage in multiple sclerosis lesions

Brain 2003 Jun;126(Pt 6):1347-1357
Lassmann H, Reindl M, Rauschka H, Berger J, Aboul-Enein F, Berger T, Zurbriggen A, Lutterotti A, Bruck W, Weber JR, Ullrich R, Schmidbauer M, Jellinger K, Vandevelde M.
Brain Research Institute and. Department of Clinical Pathology, University of Vienna, Department of Neurology, Hospital Lainz, Ludwig Boltzmann Institute for Clinical Neurobiology, Vienna, Department of Neurology, University of Innsbruck, Innsbruck, Austria, Department of Clinical Veterinary Medicine, University of Berne, Berne, Switzerland, Department of Neuropathology and. Department of Neurology, Charite, Berlin, Germany.

Recent studies on the immunopathology of multiple sclerosis revealed a heterogeneity in the patterns of demyelination, suggesting interindividual differences in the mechanism responsible for myelin destruction.

One of these patterns of demyelination, characterized by oligodendrocyte dystrophy and apoptosis, closely mimics myelin destruction in acute white matter ischaemia.

In the course of a systematic screening for virus antigen expression in multiple sclerosis brains, we identified a monoclonal antibody against canine distemper virus, which detects a cross-reactive endogenous brain epitope, highly expressed in this specific subtype of actively demyelinating multiple sclerosis lesions with little or no immunoreactivity in other active multiple sclerosis cases.

The respective epitope, which is a phosphorylation-dependent sequence of one or more proteins of 50, 70 and 115 kDa, is also expressed in a subset of active lesions of different virus-induced inflammatory brain diseases, but is present most prominently and consistently in acute lesions of white matter ischaemia.

Its presence is significantly associated with nuclear expression of hypoxia-inducible factor-1alpha within the lesions of both inflammatory and ischaemic brain diseases.

The respective epitope is liberated into the CSF and, thus, may become a useful diagnostic tool to identify clinically a defined multiple sclerosis subtype.