Sunday, 2 March 2014

Glatiramer does not neuroprotect in a stroke model


BACKGROUND: The role of the immune system in the pathophysiology of acute ischemic stroke is increasingly recognized. However, targeted treatment strategies to modulate immunological pathways in stroke are still lacking. Glatiramer acetate is a multifaceted immunomodulator approved for the treatment of relapsing-remitting multiple sclerosis. Experimental studies suggest that glatiramer acetate might also work in other neuroinflammatory or neurodegenerative diseases apart from multiple sclerosis.
FINDINGS: We evaluated the efficacy of glatiramer acetate in a mouse model of brain ischemia/reperfusion injury. 60 min of transient middle cerebral artery occlusion was induced in male C57BL/6 mice. Pretreatment with glatiramer acetate (3.5 mg/kg bodyweight) 30 min before the induction of stroke did not reduce lesion volumes or improve functional outcome on day 1.
CONCLUSIONS: Glatiramer acetate failed to protect from acute ischemic stroke in our hands. Further studies are needed to assess the true therapeutic potential of glatiramer acetate and related immunomodulators in brain ischemia.
We get accused of saying that glaterimer acetate does everything. Some people argue that it protects nerves. In this study on neurodegeneration caused by lack of blood supply, there was no protective effect detected. However, it is not clear if this is the optimum route and dose for protective effects. Further more how would this work? Protective autoimmunity? Where the white blood cells protect nerves induction. Whilst part of inflammation is repair, the evidence that this forms a dominant activity is debatable. Even if it did cause protective autoimmunity then it would probably take days to generate and the damage of the stroke would occur within that time.


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