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Stress and disease progression in multiple sclerosis and its animal models.
Neuroimmunomodulation 2006; 13(5-6):318-26N

Abstract

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.

Authors+Show Affiliations

Multiple Sclerosis Program, Department of Neurology and Cousins Center for Psychoneuroimmunology, UCLA School of Medicine, Los Angeles, CA 90095, USA, and University Hospital Hamburg-Eppendorf, Germany. sgold@mednet.ucla.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17709954

Citation

Gold, Stefan M., and Christoph Heesen. "Stress and Disease Progression in Multiple Sclerosis and Its Animal Models." Neuroimmunomodulation, vol. 13, no. 5-6, 2006, pp. 318-26.
Gold SM, Heesen C. Stress and disease progression in multiple sclerosis and its animal models. Neuroimmunomodulation. 2006;13(5-6):318-26.
Gold, S. M., & Heesen, C. (2006). Stress and disease progression in multiple sclerosis and its animal models. Neuroimmunomodulation, 13(5-6), pp. 318-26.
Gold SM, Heesen C. Stress and Disease Progression in Multiple Sclerosis and Its Animal Models. Neuroimmunomodulation. 2006;13(5-6):318-26. PubMed PMID: 17709954.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Stress and disease progression in multiple sclerosis and its animal models. AU - Gold,Stefan M, AU - Heesen,Christoph, Y1 - 2007/08/06/ PY - 2007/8/22/pubmed PY - 2007/12/6/medline PY - 2007/8/22/entrez SP - 318 EP - 26 JF - Neuroimmunomodulation JO - Neuroimmunomodulation VL - 13 IS - 5-6 N2 - 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. SN - 1021-7401 UR - https://www.unboundmedicine.com/medline/citation/17709954/Stress_and_disease_progression_in_multiple_sclerosis_and_its_animal_models_ L2 - https://www.karger.com?DOI=10.1159/000104860 DB - PRIME DP - Unbound Medicine ER -