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Nader Ghasemlou, Ph.D
Neural Plasticity Research Group
Harvard Medical School
149 13th Street, Rm. 4309
Charlestown, Massachusetts 02129-2000
TEL:
FAX: 617-724-3632
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Background
I received my B.Sc. (Hon.) and M.Sc. from Queen’s University at Kingston, Ontario specializing in neurotrophin-mediated sympathosensory axon sprouting. I then joined the laboratory of Dr. Samuel David at McGill University where I obtained a Ph.D. in Neuroscience. As part of my doctoral thesis, I studied the role of the immune response, particularly that of macrophages and chemokines/cytokines, in mediating spinal cord injury. This work led to the identification of several new candidates for the treatment of spinal cord injury. I joined the Neural Plasticity Research Group at the Massachusetts General Hospital in the fall of 2008 as a Research Fellow in Anesthesia at Harvard Medical School.
Research Interests
My current research interests are focused on the study of the molecular mechanisms underlying inflammatory pain. This work aims to identify and characterize new targets for new analgesics using microarray and multiplex analysis of the inflammatory response in the CNS and the periphery. I will focus primarily on the direct and indirect effects of chemokines and cytokines on primary sensory neurons, microglia/macrophages and/or astroglia and how they may contribute to the inflammatory pain response. In collaboration with Dr. Alexander Binshtok, I will be studying the role of inflammatory chemokines/cytokines on sensory neuron excitability using whole-cell and patch-clamp recording as well as calcium and sodium imaging techniques. We also plan to translate our results to study the effects of activation on macrophages isolated from the periphery and the CNS after inflammatory injury. As part of the inflammatory pain grant, I will also be examining the role of peripheral COX-2 in the generation of inflammatory pain phenotypes, particularly through the hematogenous immune response. The analysis of microarrays, in conjunction with Dr. Michael Costigan, to determine new pathways and specific targets of interest in several varying pain phenotypes is also underway with emphasis placed on changes occurring in the early phase of injury and disease in the central and peripheral nervous systems. I am also studying the effect of increased heat shock protein (Hsp) 27 expression in neurons after CNS injury in collaboration with Dr. Eddie Ma. Specifically, I am studying the pro-regenerative and survival effects of Hsp27 after hemisection injury using transgenic overexpressor mice recently generated in the NPRG. Work with Dr. Joachim Scholz is also underway to microglial activation following peripheral nerve injury.
Selected Publications
Ghasemlou N, Jeong SY, Lacroix S, and David S. (2007) T cells contribute to lysophosphatidylcholine-induced macrophage activation and demyelination in the CNS. GLIA 55:294-302.
Ghasemlou N, Kerr BJ, David S. (2005) Tissue displacement and impact force are important contributors to outcome after spinal cord contusion injury. Exp Neurol 196:9-17.
Ghasemlou N, Krol KM, Macdonald DR, Kawaja MD. (2004) Comparison of target innervation by sympathetic axons in adult wild type and heterozygous mice for nerve growth factor or its receptor trkA. J Pineal Res 37:230-240.
Selected Presentations
Ghasemlou N, Lopez-Vales R, Lachance C, Thuraisingam T, Radzioch D, Gaestel M, David S.
(2008) MAPK activated protein kinase 2 (MK2) controls inflammation and secondary damage after
spinal cord contusion injury. Society for Neuroscience Annual Meeting
Ghasemlou N, David S. (2007) Genotypic characterization of macrophages in the injured and
demyelinating CNS. Society for Neuroscience Annual Meeting.
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