Yet another mechanism for glatiramer acetate

From R, Eilam R, Bar-Lev DD, Levin-Zaidman S, Tsoory M, Lopresti P, Sela M, Arnon R, Aharoni R.Oligodendrogenesis and myelinogenesis during postnatal development effect of glatiramer acetate. Glia. 2014 Jan 30. doi: 10.1002/glia.22632. [Epub ahead of print]

Myelination in the mammal nervous system occurs predominantly postnatally (after birth). Glatiramer acetate (GA), a drug for the treatment for multiple sclerosis (MS), has been shown to induce immunomodulation and neuroprotection in the inflamed CNS in MS and in experimental autoimmune encephalomyelitis (EAE). Here we investigated whether GA can affect myelinogenesis and oligodendrogenesis in the developing nervous system under nonpathological conditions. Towards this end we studied myelination in mice injected daily by GA, at postnatal Days 7-21. There was  a significant elevation in the number of myelinated axons as well as in the thickness of the myelin encircling them  in spinal cords of GA-injected mice compared with their PBS (Saline= salt solution 0.9%)-injected littermates, at postnatal Day 14. Elevation in myelinated axons was detected also in the peripheral ventral roots of the motor nerves. GA induced also an increase in axonal diameter, implying an effect on the overall development of the nervous system. A prominent elevation in the amount of progenitor oligodendrocytes and their BrdU (Bromo deoxyuridine as a marker of cell division) incorporation, as well as in mature oligodendrocytes indicated that the effect of GA is linked to increased proliferation and differentiation along the oligodendroglial maturation cascade. In addition, elevation in nerve growth factors was found in the white matter of the GA-injected mice. Furthermore, a functional advantage in rotating rod test (a accelerating spinning wheel from which the animals fall when they dont have enough movement co-ordination) was exhibited by GA-injected mice over their littermates at postnatal Day 21. These cumulative findings corroborate the beneficial effect of GA on oligodendrogenesis and myelination. 



I know that this has become a bit of a theme as far as I am concerned and this irritates a number of readers, especially those using the drug but this is yet another example of a mechanism of action of this drug. 

It has had more mechanisms of action that most people have had hot dinners. Maybe this is THE action but remember in many EAE models there is no demyelination and yet Glaterimer acetate can have an impact. 


However it has been suggested to support remyelination before and saving nerves and  promoting T cell regulation and.... and....If this is the mechanism of action in MS, do we see rapid functional recovery after treatment.


We are about 40 years on from when GA was first constructed and do we know who it works. Looking forward to the next mechanism....It keeps the drug in the public eye. 


Is this a marketing ploy to keep GA uppermost in the mind?

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