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Stress and hypothalamic–pituitary–adrenal axis function in experimental autoimmune encephalomyelitis and multiple sclerosis—A review

Summary Multiple sclerosis (MS) is an inflammatory and degenerative disease of the CNS with an assumed autoimmune-mediated pathogenesis. Stressful life events have been hypothesized as potential triggers of disease exacerbation. Animal studies using experimental autoimmune encephalomyelitis (EAE), a...

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Bibliographic Details
Published in:Psychoneuroendocrinology 2007-07, Vol.32 (6), p.604-618
Main Authors: Heesen, C, Gold, S.M, Huitinga, I, Reul, J.M.H.M
Format: Article
Language:English
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Summary:Summary Multiple sclerosis (MS) is an inflammatory and degenerative disease of the CNS with an assumed autoimmune-mediated pathogenesis. Stressful life events have been hypothesized as potential triggers of disease exacerbation. Animal studies using experimental autoimmune encephalomyelitis (EAE), as a model for MS, suggest that decreased hypothalamic–pituitary–adrenal (HPA) function may play a role in the increased susceptibility and severity of the disease. Histopathological studies of the hypothalamus point to disturbances in corticotropin-releasing hormone (CRH) regulation as a result of MS lesions in this area. Functional endocrine tests (e.g., the combined Dexamethasone–CRH test) showed a disturbed negative feedback after steroid application in MS patients. Hyper- and hypoactivity of the HPA axis, have been described to be associated with more severe courses. This paper presents an overview of the evidence for a role of HPA dysfunction in EAE and MS based on stress-experimental studies.
ISSN:0306-4530
1873-3360
DOI:10.1016/j.psyneuen.2007.05.002