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Multiple sclerosis (MS) is one of the most common neurological demyelinating diseases of the human central nervous system (CNS). The etiology and pathogenesis of the disease are not well understood. The process of demyelination is believed to involve a T-cell-mediated autoimmune phenomenon triggered and exacerbated by one or more viral infections. The primary target of MS is believed to be either myelin itself (myelinopathy) or the myelin-forming cells, the oligodendrocytes (oligodendrogliopathy). Recently, however, gray matter involvement and axonal injury (axonopathy) present in normal-appearing white matter have been demonstrated in MS, and it has been hypothesized that they are responsible for long-term disability. In our laboratory, we are focusing on understanding specific aspects of oligodendrocyte death and myelin damage that illuminates the complex interplay of cellular mechanisms involved in the process of demyelination.
To pursue our research goals we use two different mouse model systems to study how individual CNS cell can damage and contribute to demyelination process in MS. These model systems are: (i) Mouse hepatitis virus induced demyelinating model, and (ii). Experimental Autoimmune Encephalomyelitis (EAE) model.
For our studies we use a combination of experimental techniques that come from basic and advanced virology, cell biology, molecular biology and immunology. We perform our in vivo experiments in mice and in vitro experiments in primary glial cell culture. Commonly used techniques are: isolation of primary neural cells, immunofluorescence, immunohistochemistry, in situ hybridization, cloning, Q-PCR, viral plaque assay, targeted RNA recombination for recombinant (including fluorescent tagged) virus generation, isolation and purification of peripheral immune cells and macrophages, flow cytometric analysis of primary cells. We also plan to use laser capture microscopy and time lapse in vivo imaging of fluorescent tagged viruses.
Our work aims to understand cellular pathways of demyelination in animal models to infer mechanisms of Multiple Sclerosis in humans. It is hoped that the enhanced understanding of the neurodegenerative processes will allow us to identify new therapeutic targets for MS.
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