Limited effects of glatiramer acetate in the high-copy number hSOD1-G93A mouse model of ALS.
Experimental Neurology(2007)
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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