个人简介
Stephen Waxman exemplifies the bridge between basic research and clinical medicine. He is the Bridget Flaherty Professor of Neurology, Neurobiology, and Pharmacology at Yale University. He served as Chairman of Neurology at Yale from 1986 until 2009. He founded and is Director of the Neuroscience & Regeneration Research Center at Yale. He also holds an appointment as Visiting Professor at University College London. Prior to moving to Yale, Dr. Waxman worked at Harvard, MIT, and Stanford.
Dr. Waxman received his BA from Harvard, and his MD and PhD degrees from Albert Einstein College of Medicine. His research, which uses tools from the “molecular revolution” to find new therapies that will promote recovery of function after injury to the brain, spinal cord, and peripheral nerves, has received international recognition.
Dr. Waxman’s research has defined the ion channel architecture of nerve fibers, and demonstrated its importance for axonal conduction (Science, 1985). He demonstrated increased expression of sodium channels in demyelinated axons (Science, 1982), identified the channel isoforms responsible for this remarkable neuronal plasticity which supports remission in multiple sclerosis (PNAS, 2004), and delineated the roles of sodium channels in axonal degeneration (PNAS, 1993). He has made pivotal discoveries that explain pain after nerve injury. Most recently, in translational leaps from laboratory to humans, he carried out molecule-to-man studies combining molecular genetics, molecular biology, and biophysics to demonstrate the contribution of ion channels to human pain (Trends in Molec.Med, 2005; PNAS, 2006), led an international coalition that identified sodium channel mutations as causes of peripheral neuropathy (PNAS, 2012) and has used atomic-level modeling to advance pharmacogenomics (Nature Comm., 2012). A new class of pain medications without central side-effects or addictive potential, based on his work, is currently in clinical trials.
Dr. Waxman has published more than 600 scientific papers. He has as edited nine books, and is the author of Spinal Cord Compression and of Clinical Neuroanatomy (translated into eight languages). He has served on the editorial boards of many journals including The Journal of Physiology, Brain, Annals of Neurology, Trends in Neurosciences, Nature Reviews Neurology, and Trends in Molecular Medicine, and is Editor-in-Chief of Neuroscience Letters. He has trained more than 150 academic neurologists and neuroscientists who lead research teams around the world.
A member of the Institute of Medicine of the National Academy of Sciences, Dr. Waxman’s many awards include the Tuve Award (NIH), the Distinguished Alumnus Award (Albert Einstein College of Medicine), the Dystel Prize and Wartenberg Award (American Academy of Neurology), and the Middleton Award and Magnuson Award of the Veterans Administration. He received the Annual Prize of the British Physiological Society, an honor he shares with his heroes, Nobel Prize laureates Andrew Huxley, John Eccles, and Alan Hodgkin.
MD Albert Einstein College (1972)
PhD Albert Einstein College (1970)
Postdoctoral Fellow MIT
Resident Boston City Hospital
Clinical Fellow Harvard Medical School
近期论文
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Gain-of-function NaV1.8 mutations in painful neuropathy.
Faber, C.G., Lauria, G., Merkies, I.S.J., Cheng, X., Han, C., Ahn, H-S., Persson, A-K., Hoeijmakers, J.G.J., Gerrits, M.M., Pierro, T., Lombardi, R., Kapetis, D., Dib-Hajj, S.D., and Waxman, S.G. Gain-of-function NaV1.8 mutations in painful neuropathy. PNAS, 109:19444-19449, 2012. PMID: 23115331
The NaV1.7 sodium channel: from molecule to man.
Dib-Hajj, S.D., Yang, Y., Black, J.A., Waxman, S.G. The NaV1.7 sodium channel: from molecule to man. Nat Rev Neurosci, 14(1): 49-62, 2012. PMID: 23232607
Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(V)1.7 mutant channel.
Yang, Y., Dib-Hajj, S.D., Zhang, J., Zhang, Y., Tyrrell, L., Estacion, M., and Waxman, S.G. Structural modeling and mutant cycle analysis predict pharmacoresponsiveness of a NaV1.7 mutant channel, Nature Comm., 3: 1186, 2012. PMID 23149731
Sodium Channels and neuroprotection in MS: current status
Waxman, S.G. (2008) Sodium Channels and neuroprotection in MS: current status., Nature Clinical Neurology, 4, 159-170
Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromas.
Black, J.A., Nikolajsen, L., Kroner, K., Jensen, T.S., and Waxman, S.G., Multiple sodium channel isoforms and MAP kinases are present in painful human neuromas. Annals of Neurology, 64(6): 644-53, 2008. PMID: 19107992.
Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons.
Rush, A.M., Cummins, T.R., Waxman, S.G. Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons. J. Physiol. 579:1-14, 2007. PMID: 17158175
Channel, neuronal, and clinical function in sodium channelopathies: From genotype to phenotype.
Waxman, S.G., Channel, neuronal, and clinical function in sodium channelopathies: From genotype to phenotype. Nature Neuroscience, 10:405-410, 2007. PMID: 17387329
Axonal conduction and injury in multiple sclerosis: the role of sodium channels.
Waxman, S.G. Axonal conduction and injury in multiple sclerosis: the role of sodium channels. Nature Rev. Neurosci., 5: 932-942, 2006. PMID: 17115075
Pharmacotherapy for pain in a family with inherited erythromelalgia guided by genomic analysis and functional profiling.
Geha, P., Yang, Y., Estacion, M., Schulman, B.R., Tokuno, H., Apkarian, A.V., Dib-Hajj, S.D., Waxman, S.G. Pharmacotherapy for pain in a family with inherited erythromelalgia guided by genomic analysis and functional profiling. JAMA Neurol., in press, 2016. PMID: 27088781
Pharmacological reversal of pain phenotype in iPSC-derived sensory neurons and human subjects with inherited erythromelalgia,
Cao, L., Nitzsche, N., McDonnell, A., Alexandrou, A., Saintot, P-P., Loucif, A.J.C., Brown, A.R., Young, G., Mis, M., Randall, A., Waxman, S.G., Stanley, P., Kirby, S., Tarabar, S., Gutteridge, A., Butt, R., McKernan, R.M., Whiting, R., Ali, Z., Bilsland, J., Stevens, E.B. Pharmacological reversal of pain phenotype in iPSC-derived sensory neurons and human subjects with inherited erythromelalgia, Science Translational Medicine, 8(335): 335ra56, 2016. PMID: 27099175
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