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Please use this identifier to cite or link to this item: http://hdl.handle.net/1993/4516

Title: NeuroImmune modulation of multiple sclerosis via the dorsal root ganglia
Authors: Melanson, Maria
Supervisor: Namaka, Mike (Pharmacy)
Examining Committee: Kreillaars, Dean (Medical Rehabilitation) Shay, Barbara (Medical Rehabilitation)
Graduation Date: May 2011
Keywords: TNS alpha, tumor necorsis factor, dorsal root ganglia, EAE
Issue Date: 11-Apr-2011
Citation: Melanson, Maria (2008). Axotomy-induced up-regulation of tumor necrosis factor-alpha in the dorsal root ganglia. Neurol Res. Jul;30(6):623-31, Epub 2008 May 16.
Abstract: Background: Multiple sclerosis (MS) is a chronic, neurological disease characterized by targeted destruction on central nervous system (CNS) myelin. The autoimmune theory is the most widely accepted explanation of disease pathology. Circulating Th-1 cells become activated by exposure to CNS-specific antigens such as myelin basic protein. The activated Th-1 cells secrete inflammatory cytokines, which are pivotal for inflammatory responses. We hypothesize that enhanced production of inflammatory cytokines triggers cellular events within the dorsal root ganglia (DRG) and/or spinal cord, facilitating the development of neuropathic pain (NPP) in MS. NPP, the second worst disease-induced symptom suffered by patients with MS, is normally regulated by DRG and/or spinal cord. Objective: To determine gene and protein expression levels of tumor necrosis factor-alpha (TNF ) within DRG and/or spinal cord in an animal model of MS. Methods: Experimental autoimmune encephalomyelitis (EAE) was induced in adolescent female Lewis rats. Animals were sacrificed every 3 days post-disease induction. DRG and spinal cords were harvested for protein and gene expression analysis. Results: We show significant increases in TNF expression in the DRG and of EAE animals at peak disease stage, as assessed by clinical symptoms. Conclusion: Antigen-induced production of inflammatory cytokines such as TNF within the DRG identifies a potential noel mechanism for MS-induced NPP.
URI: http://hdl.handle.net/1993/4516
Appears in Collection(s):FGS - Electronic Theses & Dissertations (Public)

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