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From the Institute of Clinical Neuroimmunology, Ludwig-Maximilians-University, Klinikum Grosshadern, Munich, Germany, and the Department of Neuroimmunology, Max Planck Institute of Neurobiology, Martinsried, Germany.
Address correspondence and reprint requests to Dr. Reinhard Hohlfeld, Institute of Clinical Neuroimmunology, Klinikum Grosshadern, Marchioninistr. 15, D-81377 Munich, Germany reinhard.hohlfeld{at}med.unimuenchen.de
Inflammatory responses in the CNS have usually been perceived to cause or contribute to neuron injury. However, emerging evidence suggests that inflammatory reactions can also be neuroprotective. The nervous and immune systems employ overlapping mechanisms and shared mediators that promote cross-talk between the two systems. Immune cells, for example, produce not only neurodestructive molecules but also factors that can support neuroaxonal growth, survival, and plasticity. This might explain why inflammatory reactions may contribute to both injury and protection of neurons. The dual role of CNS inflammation also has important therapeutic implications that are only beginning to be explored.
This supplement was supported by an educational grant from Teva Neuroscience. BioScience Communications contributed to the editorial refinement of this article and to the production of this supplement. Authors may have accepted honoraria for their supplement contributions.
Disclosure:. R.H. and E.M. have received grant support and consulting fees from Schering, Teva, Serono, and Biogen-Idec. M.K. has nothing to report.
Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represents the opinions of the authors and is not endorsed by nor does it reflect the views of the American Academy of Neurology, Editorial Board, Editor-in-Chief, or Associate Editors of Neurology.
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