Treatment of early RRMS with Alemtuzumab reduces relapses and the accumulation of disability compared to interferon β. Remarkably PwMS treated with alemtuzumab experienced an improvement in disability at 6 months that was sustained for at least 3 years in comparison to those treated with interferon β.
Critics have poopooed this observation as the study was single-blinded and liable to unblinding; i.e. only the evaluating neurologist is blinded to what the study subject received in the study. Due to infusion reactions from Alemtuzumab it is not possible to do double-blinded studies with the agent; i.e. studies in which the evaluating neurologist and study subjects do no know what they have received.
In an additional analysis of the phase 2 trial data it appears that the participants with no clinical disease activity immediately before treatment, or any clinical or radiological disease activity during the study trial, were noted to improve after Alemtuzumab but not following interferon β treatment. This would suggest that disability improvement after Alemtuzumab may not simply be due to its anti-inflammatory effects.
This statement is subject to the same criticisms levelled at the whole study; but despite these criticisms this would be the first treatment in MS to offer such a benefit. No wonder PwMS are so excited about the prospect of receiving this therapy.
Preliminary experiments hint that Alemtuzumab stimulates white blood cells to produce growth factors that promote survival of nerve cells and enhanced oligodendrocyte (cells that produce myelin) function. This data will need to be replicated and shown to be relevant in patients treated with Alemtuzumab.
The implications of this research for PwMS cannot be overemphasised; at last a possible treatment with the potential to promote recovery.
Jones et al Brain. 2010 Aug;133(Pt 8):2232-47. Epub 2010 Jul 21.
3 thoughts on “Improvement in MS disability after Alemtuzumab”
Does the last paragraph in your blog imply that there could be benefits for people with progressive forms of MS, too?
Yes, it all depends on timing and the ability to harness recovery mechanisms.
I thought the team at Addenbrook's tried Campath on SPMS patients, but it wasn't a success. My big hope for stopping / radically slowing neuro-degeneratation was Lamotrigine – but it didn't deliver. If a treatment could be found that stopped neuro-degenration and another which promoted the repair of myelin and axons then we would be on to something. Anti-lingo anti-body looks interesting (currently Phase 1 trial) – but so many of the promising drugs in trial disappoint!!!!!!!!