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Multiple sclerosis - the silent saboteur

29 July 2013

Scope 51

Multiple sclerosis affects 1 in 1,400 New Zealanders.

Multiple sclerosis (MS) is characterised by immune-mediated nerve degeneration, leading to impaired vision, coordination and paralysis. There is no cure. While disease-modifying drugs are available, they are often effective in only a subset of MS patients.

Malaghan Institute Research Associate Dr Anne La Flamme leads a research programme investigating the basic immune cell biology of MS, to understand how to optimise currently available therapies and to develop novel agents that are more effective at treating patients who do not respond to current MS therapies.

One commonly prescribed agent is glatiramer acetate (GA, also known as Copaxone), which is used to treat relapsing-remitting MS. Recent work by Malaghan researchers and other MS research groups using mouse models of MS, has shown that GA alters the activation state of monocytes – a type of white blood cell.

In collaboration with Dr Scott Harding and Dr David Abernathy from Wellington Hospital, PhD student Dr Delgersetseg Chuluundorj undertook a detailed analysis of the physiological effects of GA on the activation of monocytes from patients with MS, and from healthy volunteers. This information will help form the basis of a model that could be used to predict if a patient will respond to GA treatment.

Intravenous gammaglobulin is another immune-modifying therapy used to treat MS, albeit with limited success. Interestingly, Dr Chulunndorj’s studies showed that while the effects of intravenous gammaglobulin on monocyte activation were similar, but also distinct, to those induced by GA, the two compounds worked well together. This has positive implications for patients who do not respond to either agent alone.

Complementing this work is that of PhD student Sarrabeth Stone (pictured), who has been investigating how the above agents affect the activation of microglia – a type of immune cell related to monocytes that is found specifically in the brain. It is these cells that are thought to mediate the nerve damage associated with the progressive form of MS, for which there is currently no treatment.

We would like to acknowledge all of the MS patients who graciously donated their blood for this research. This work would not have been possible without their support.

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