Chronic relapsing experimental allergic encephalomyelitis: An experimental model of multiple sclerosis

Wı́sniewski, Henryk M.; Keith, A.B.

doi:10.1002/ana.410010207

Cited by 267 publications

(45 citation statements)

References 6 publications

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“…There is thus no convincing evidence that excess zinc contributes to the known role of risk factors such as genetics, sex, and geography in the etiology of this immunologically based myelin disorder of the nervous system. Animal models with CNS pathology analogous to MS are available (363), which might be used to examine the effect of increased zinc intake on disease progression.…”

Section: Neurological Function and Excessmentioning

confidence: 99%

Zinc: Health Effects and Research Priorities for the 1990s

Walsh¹,

Sandstead²,

Prasad³

et al. 1994

Environmental Health Perspectives

156

225

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This review critically summarizes the literature on the spectrum of health effects of zinc status, ranging from symptoms of zinc deficiency to excess exposure. Studies on zinc intake are reviewed in relation to optimum requirements as a function of age and sex. Current knowledge on the biochemical properties of zinc which are critical to the essential role of this metal in biological systems is summarized. Dietary and physiological factors influencing the bioavailability and utilization of zinc are considered with special attention to interactions with iron and copper status. The effects of zinc deficiency and toxicity are reviewed with respect to specific organs, immunological and reproductive function, and genotoxicity and carcinogenicity. Finally, key questions are identified where research is needed, such as the risks to human health of altered environmental distribution of zinc, assessment of zinc status in humans, effects of zinc status in relation to other essential metals on immune function, reproduction, neurological function, and the cardiovascular system, and mechanistic studies to further elucidate the biological effects of zinc at the molecular level. - There is considerable evidence that zinc deficiency in humans is a serious worldwide problem and outweighs the potential problem of accidental, self-imposed, or environmental exposure to zinc excess. Acute deficiency (1) and chronic deficiency (2) are well-known entities in human populations and are probably much more common than generally recognized. The importance of zinc for human health was first documented in 1963 (3) Telephone (617) (617) 638-4329. E-mail: ctwalsh~bu.edu renal disease, and other chronically debilitating diseases are now known to be predisposing factors for zinc deficiency in humans (4).Zinc deficiency is reflected in clinical syndromes which affect men and women of all ages and all socioeconomic and cultural classes in the United States. It is neither prevalent in any specific area of the United States nor associated with any specific or definitive biochemical marker, which can make its identification difficult and confusing. Its presence is manifested by a wide spectrum of symptoms, from acute, life threatening problems to mild subclinical or marginal disorders which may only vaguely disturb well being. The acute problems are often seen in profoundly ill patients treated in hospitals, whereas subclinical problems may be so vague that patients seek assistance outside traditional medical practice.Based upon clinical data and using traditional, epidemiologic techniques, Henkin and Aamodt (5) have reclassified zinc deficiency into three syndromes; these are a) acute, b) chronic, and c) subacute zinc deficiency. Acute zinc deficiency is relatively uncommon and follows parenteral hyperalimentation or oral L-histidine administration. Chronic zinc deficiency is more common, usually resulting from chronic dietary lack of zinc. Subacute or latent zinc deficiency is the most common of these syndromes. It is estimated that there are 4...

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Section: Neurological Function and Excessmentioning

confidence: 99%

Zinc: Health Effects and Research Priorities for the 1990s

Walsh¹,

Sandstead²,

Prasad³

et al. 1994

Environmental Health Perspectives

156

225

View full text Add to dashboard Cite

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“…In EAE, the perivascular inflammatory infiltrate leads to damage of the myelin sheath surrounding the nerve although the myelin-producing oligodendrocytes can remyelinate [50]. In contrast in EAU, the damage to the photoreceptor cells is irreversible as these cells are not regenerated.…”

Section: Reverstbility Of Diseasementioning

confidence: 99%

Experimental autoimmune uveoretinitis (EAU)versusexperimental allergic encephalomyelitis (EAE): a comparison of T cell-mediated mechanisms

Calder¹,

Lightman²

1992

Clinical and Experimental Immunology

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SUMMARYEAU is a model of ocular inflammatory disease. EAU resembles another T cell-mediated autoimmune disease-experimental allergic encephalomyelitis-since both have increased expression of MHC class II molecules in the target tissue, can be adoptively transferred by activated CD4*-T cells and are inhibited by cyclosporin A. The immunological findings will be compared to find out if the same cellular mechanisms are involved in both diseases.

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“…Morphologically, CR-EAE has the two characteristic features of MS lesions, namely the presence of recent and old demyelinating plaques and the periventricular distribution of lesions. Moreover, in both CR-EAE and MS, advanced disease is associated with chronic rather than acute lesions (5). CR-EAE can, therefore, be used as a more reliable model to study therapies for CNS-targeted autoimmune disorders.…”

mentioning

confidence: 99%