NN0706 NV.indd
نویسنده
چکیده
This study raises the exciting possibility that mimicking the effects of fractalkine may control microglia activation and provide neuroprotection in a variety of neurological diseases featuring neuroinflammation. Some success has already been achieved in preclinical models of neurodegenerative diseases by targeting neuroinflammation through the inhibition of microglial activation with agents like minocycline, dextromethorphan or vasoactive intestinal peptide, or by suppression of specific microglial toxic effectors using iNOS antagonists or nonsteroidal antiinflammatory drugs1. Among these, several (for example, minocycline) are currently being tested in clinical trials for Parkinson disease and ALS. We may envision that fractalkine agonists that can permeate the blood-brain barrier, should they become available, would be prime candidates in neuroprotective clinical trials for these incurable neurodegenerative diseases. However, stimulation of the fractalkine pathway may be a double-edged sword if not finely tuned, as it may also aggravate atherosclerosis15. Thus, fractalkine-based human clinical trials will need to begin by determining how these drugs may affect susceptibility to cardioand cerebrovascular accident.
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NN1207 NV.indd
5. Bayer, H.M. & Glimcher, P.W. Neuron 47, 129–141 (2005). 6. Tobler, P.N., Fiorillo, C.D. & Schultz, W. Science 11, 1642–1645 (2005). 7. Pessiglione, M. et al. Nature 442, 1042–1045 (2006). 8. Watkins, C. Learning from Delayed Rewards. Thesis, Cambridge Univ. (1989). 9. Morris, G., Nevet, A., Arkadir, E. & Bergman, H. Nat. Neurosci. 9, 1057–1063 (2006). 10. O’Doherty, J. et al. Science 304, 45...
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