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Limited effects of glatiramer acetate in the high-copy number hSOD1-G93A mouse model of ALS.

Experimental Neurology(2007)

Cited 22|Views16
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Abstract
In amyotrophic lateral sclerosis (ALS), an involvement of the immune system in the degenerative processes has been shown in both humans and the transgenic SOD1-G93A mice. We previously showed that Glatiramer acetate (also known as copolymer-1; COP-1; Copaxone®) improves motor function and extends survival times in an inbred strain of ALS mice probably by interacting with pro-inflammatory TH lymphocytes. In the course of this study we tested whether these beneficial effects could be reproduced by repeated vaccination of animals with COP-1 without co-administration of complete Freund's adjuvant. In an outbred strain we could not demonstrate a positive effect of COP-1 on survival times, but found a significant improvement of motor performance during the late stage of disease and a moderate decrease of the production of the inflammatory cytokines interferon-γ and IL-4 by T lymphocytes isolated from the mice's spleen. In conclusion, the effects of COP-1 in the applied hybrid strain displaying a faster disease progression were less pronounced than in the earlier tested inbred strain of ALS mice.
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Key words
Amyotrophic lateral sclerosis,Glatiramer acetate,Copaxone®,Cu/Zn-superoxide dismutase,SOD1-G93A
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