Remyelination supplies Energy

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Mitochondrial content within axons increases following demyelination in the central nervous system, presumably as a response to the changes in energy needs of axons imposed by redistribution of sodium channels. Myelin sheaths can be restored in demyelinated axons and remyelination in some multiple sclerosis lesions is extensive, while in others it is incomplete or absent. The effects of remyelination on axonal mitochondrial content in multiple sclerosis, particularly whether remyelination completely reverses the mitochondrial changes that follow demyelination, are currently unknown. In this study, we analysed axonal mitochondria within demyelinated, remyelinated and myelinated axons in post-mortem tissue from patients with multiple sclerosis and controls, as well as in experimental models of demyelination and remyelination, in vivo and in vitro. Immunofluorescent labelling of mitochondria (porin, a voltage-dependent anion channel expressed on all mitochondria) and axons (neurofilament), and ultrastructural imaging showed that in both multiple sclerosis and experimental demyelination, mitochondrial content within remyelinated axons was significantly less than in acutely and chronically demyelinated axons but more numerous than in myelinated axons. The greater mitochondrial content within remyelinated, compared with myelinated, axons was due to an increase in density of porin elements whereas increase in size accounted for the change observed in demyelinated axons. The increase in mitochondrial content in remyelinated axons was associated with an increase in mitochondrial respiratory chain complex IV activity. In vitro studies showed a significant increase in the number of stationary mitochondria in remyelinated compared with myelinated and demyelinated axons. The number of mobile mitochondria in remyelinated axons did not significantly differ from myelinated axons, although significantly greater than in demyelinated axons. Our neuropathological data and findings in experimental demyelination and remyelination in vivo and in vitro are consistent with a partial amelioration of the supposed increase in energy demand of demyelinated axons by remyelination.
One reader thought this article was the bees kness. Getting enough energy t nerves is central to their and any other cells health

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MouseDoctor

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  • Yes, I think this is the bees knees.

    To summarize, demyelination causes a change in axons such that an increase energy demand is required to maintain signal conduction. Over time the increased energy demand eventually kills the axon as well as the neuron itself.

    I suspect this increased energy demand is related to fatigue that is so prominent in MSers.

    So, if you can prevent demyelination from occuring you may not experince this type of axonal dysfunction, but if it happens we need a way to prevent the decline of the neuron.

    Incidentally, there are a range of diseases that appear to be related to the axonal dysfunction known as mitochondrial diseases:

    http://www.umdf.org/site/pp.aspx?c=8qKOJ0MvF7LUG&b=7934627

    However, these diseases appear to be a result of inate mitochondrial dysfunction rather than processes that create changes to mitochondrial function. At any rate, people working on these two different disease types may benefit from the knowledge obtained in their different fields of investigation.

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