Wednesday, 10 July 2013

Remyelination the True Regeneration

Crawford AH, Chambers C, Franklin RJ. Remyelination: The True Regeneration of the Central Nervous System. J Comp Pathol. 2013 Jul 4. doi:pii: S0021-9975(13)00085-6. 10.1016/j.jcpa.2013.05.004. [Epub ahead of print]

The myelin sheath, generated by oligodendrocytes in the central nervous system (CNS), is crucial to neuronal function, enabling rapid propagation of nerve impulses and providing trophic support to the axon. Remyelination is the default response to myelin damage. Oligodendrocyte precursor cells, distributed throughout both the grey and white matter of the CNS, are activated in response to myelin injury, undergoing proliferation, migration to the site of damage and differentiation into mature myelinating oligodendrocytes. The end result is complete reconstruction of the area of myelin loss. However, this remarkable regenerative capacity of the CNS becomes less efficient with age and can show clinically significant failure in diseases such as multiple sclerosis. Without the myelin sheath, neuronal function and survival is compromised, leading to axonal degeneration and progressive deterioration in neurological function. Therapies to enhance remyelination could offer a means to prevent the neurological decline of chronic demyelinating disease. In order to develop such therapies, a detailed understanding of the process of remyelination, the major cellular players involved and the mechanisms of remyelination failure is needed. As the intricacies of remyelination continue to be unravelled, effective remyelination therapies are ever closer to becoming a reality.

So more upbeat views from Prof Franklinstein

7 comments:

  1. That's assuming there are still axons left to remyelinate of course.

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    1. Endogenous remyelination occurs but with a reduced thickness around the axon. Eventually this repair is inadequate and there is loss of the axon. Maybe there needs to be more focus on the inside out theory that suggests axonal attack is driving the disease process preventing efficient remyelination.

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    2. That's where we're coming from too. Save the axon so the potential is there to remyelinate.

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    3. Is it posible to image/ measure the damage done to the axons ?

      Regards as always.

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    4. Re: "s it posible to image/ measure the damage done to the axons ?"

      Yes, with MRI. The markers we use are black holes on T1-weighted MRI,MR-spectroscopy that shows a loss of a metabolite called NAA that is relatively specific to nerves and axons and atrophy (shrinkage of the brain, spinal cord or gray matter). A new technique is OCT or optical coherence tomography that measures the thickness of the nerve fibre layer on the retina. You can also use evoked potentials; the size of the evoked potentials is an indication of how many axons are working in that pathway. My favorite is CSF neurofilament levels; the greater the levels the more axons are being damaged and lost.

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  2. Re "upbeat views from Prof Franklinstein?"

    What are your views? Are "effective remyelination therapies" close to reality?

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  3. For people on trials close, for general circulation the time it takes to do phase1/11 phase iii and then registration and then NICE

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