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All well and good, but this has all been shown in cell lines and thus its clinical relevance remains suspect.However the authors head off this criticism by testing the compound in the R transgenic mouse model of HD a mouse in which a truncated form of htt with CAG repeats is expressed.They do this by either injecting the compound intraperitoneally or infusing it via osmotic minipumps intracerebroventricularly.This manoeuvre ameliorates some of the systemic symptoms of the mice, for example increasing survival, maintaining weight, and improving the motor deficits whilst histologically reducing the accumulation of aggregates.This paper represents a tour de force of experiments and suggests that oligomerization may be a critical pathogenic event in this and other polyglutamine disorders.Until then, patients and society will continue to face the huge emotional and economic costs of disability due to persistent demyelination.Remyelination is the answer, although that is easier said than done.One school of thought is that cells should be injected into the MS brain that have the capacity to migrate, divide and remyelinate but safely, without going where they should not and without forming tumours.A cell with all these NSI-189 properties has yet to be identified.This humble cell has the great attraction for human therapeutic purposes that it can easily be harvested from the patients own olfactory bulb.In animal studies, olfactory ensheathing cells clearly remyelinate and so now research is turning to the practical issues which must be faced before translating to the clinic.This paper addresses the apparently mundane question of whether it matters if the transplanted olfactory ensheathing cells are contaminated by meningeal cells during the olfactory bulb dissection.At last a really useful independent analysis of the interferonbeta trials in relapsingremitting multiple sclerosis has been done.As well as humbling the extravagant claims for this class of drug, the authors also criticise the trials comprehensively.For instance, there was evidence for a treatment effect at year one, but there were insufficient data at year two to judge whether this continued.The authors Toltrazuril approached this problem with a sensitivity analysis assuming a worst and best case scenario.If it was assumed that dropouts had higher disease activity than those who remained in the study then the systematic review did not find any significant effect of interferonbeta on relapse rate in year two or on the overall accumulation of disability.One such molecule is complex, expressed on the activated lymphocy tes.Therefore blocking the interaction of, found on endothelial cells should prevent migration of pathogenic T cells into the brain.The hope would be and to some extent this has already been demonstrated in animal experiments and pilot clinical studies that such blockade of the VLA and VCAM interaction may reduce disease activity in inflammatory CNS diseases.Patients with both relapsingremitting and secondary progressive MS were included in the study.MRI evidence of new lesions were substantially less in the treatment groups. Wellbeing, measured by a visual analogue test, was improved in the treatment groups but worsened in the placebo group.However antibodies to natalizumab developed in of those in the natalizimab groups and the emergence of these antibodies was dose dependent.

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