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- W2314658811 abstract "Major neurological deficits in multiple sclerosis (MS) can arise from neuroinflammation per se, aside from demyelination, but the mechanisms remain unclear. Neuropathological studies have revealed that MS lesions can have hypoxia-like properties, including the expression of hypoxia-related antigens, raising the possibility that some deficits may be due to tissue hypoxia and an energy crisis. We have shown that the spinal cord of rats with active experimental autoimmune encephalomyelitis (EAE; a model of MS) can be hypoxic, and that the hypoxia can be reversed by inspiring oxygen-enriched air. Here we have explored whether oxygen therapy can also ameliorate neurological deficits in EAE. We found that in comparison with room air controls, both short-term treatment (1 h, 100% normobaric oxygen) and continued treatment (24 h at 75%) were effective in reducing the neurological deficit during the first peak of active EAE induced in Dark Agouti rats by immunisation with recombinant myelin oligodendrocyte glycoprotein. The prompt improvement, achieved within 1 h, was reversed when rats were returned to room air for another hour, underlining a specific, transient beneficial effect of oxygen exposure. The continuous, 24 h, treatment was applied on either the first, second or third day from disease onset, and oxygen was found to reduce neurological deficits at each stage, compared with controls. To avoid potential complications in interpretation arising from demyelination we have also studied animals with non-demyelinating, passive EAE induced by the systemic administration of encephalitogenic T cells. We reveal that, as in active EAE, the spinal cord of affected animals is hypoxic, providing a sufficient explanation for the concurrent neurological deficits. Neurons and oligodendrocytes are particularly affected. We conclude that tissue hypoxia is an important but currently overlooked cause of severe neurological deficits in neuroinflammatory disease, and that oxygen administration can promptly ameliorate the deficits." @default.
- W2314658811 created "2016-06-24" @default.
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- W2314658811 date "2014-10-01" @default.
- W2314658811 modified "2023-09-23" @default.
- W2314658811 title "Loss of function due to neuroinflammation: A role for oxygen therapy?" @default.
- W2314658811 doi "https://doi.org/10.1016/j.jneuroim.2014.08.360" @default.
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