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      Stress and Disease Progression in Multiple Sclerosis and Its Animal Models

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          Since the first description of multiple sclerosis (MS) by Charcot, stress has been hypothesized to be a potential trigger of relapses. In recent years, data from observational studies in MS patients have provided some support for an association between stress and MS relapses. Furthermore, studies employing the MS animal model experimental autoimmune encephalomyelitis have shown that certain stressors can exacerbate the disease if administered prior to disease induction. Several lines of research have explored the 2 major stress response systems – the hypothalamic-pituitary-adrenal axis and the autonomic nervous system – and their relation to disease course in MS and experimental autoimmune encephalomyelitis. These studies provide evidence that insensitivity of the immune system to signals from these systems may play a role in inflammatory events. These findings can be integrated into a biological model of stress response system alterations in MS.

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          Most cited references 40

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          Heterogeneity of multiple sclerosis pathogenesis: implications for diagnosis and therapy.

          Multiple sclerosis is a chronic inflammatory disease of the nervous system in which a T-cell-mediated inflammatory process is associated with destruction of myelin sheaths. Although demyelination is the primary event, axons are also destroyed in the lesions, and the loss of axons correlates with permanent functional deficit. Here, we discuss evidence that demyelination and axonal destruction follow different pathogenetic pathways in subgroups of patients. This might, at least in part, explain the heterogeneity in genetic susceptibility, clinical presentation and response to treatment observed between individuals.
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            New concepts in the immunopathogenesis of multiple sclerosis.

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              Axonal and neuronal degeneration in multiple sclerosis: mechanisms and functional consequences.

               C Bjartmar,  B Trapp (2001)
              Renewed interest in axonal injury in multiple sclerosis has significantly shifted the focus of research into this disease toward neurodegeneration. During the past year magnetic resonance and morphologic studies have continued to confirm and extend the concept that axonal transection begins at disease onset, and that cumulative axonal loss provides the pathologic substrate for the progressive disability that most long-term MS patients experience. Although inflammation and chronic demyelination are probable causes of axonal transection, little is known about the molecular mechanisms that are involved. The view that MS can also be considered an inflammatory neurodegenerative disease has important clinical implications for therapeutic approaches, monitoring of patients, and future treatment strategies.

                Author and article information

                S. Karger AG
                August 2007
                22 August 2007
                : 13
                : 5-6
                : 318-326
                aMultiple Sclerosis Program, Department of Neurology and Cousins Center for Psychoneuroimmunology, UCLA School of Medicine, Los Angeles, Calif., USA; bDepartment of Neurology, University Hospital Hamburg-Eppendorf, Hamburg, Germany
                104860 Neuroimmunomodulation 2006;13:318–326
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 1, References: 56, Pages: 9


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