Yes, the article you posted is saying what I was above and in previous posts. That article links you to this one (posted above):
Ann Neurol. 2006 Jan 3; [Epub ahead of print] Related Articles, Links
Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients.
Dutta R, McDonough J, Yin X, Peterson J, Chang A, Torres T, Gudz T, Macklin WB, Lewis DA, Fox RJ, Rudick R, Mirnics K, Trapp BD.
Department of Neurosciences, Lerner Research Institute.
OBJECTIVE: Degeneration of chronically demyelinated axons is a major cause of irreversible neurological disability in multiple sclerosis (MS) patients. Development of neuroprotective therapies will require elucidation of the molecular mechanisms by which neurons and axons degenerate. METHODS: We report ultrastructural changes that support Ca2+-mediated destruction of chronically demyelinated axons in MS patients. We compared expression levels of 33,000 characterized genes in postmortem motor cortex from six control and six MS brains matched for age, sex, and postmortem interval. As reduced energy production is a major contributor to Ca2+-mediated axonal degeneration, we focused on changes in oxidative phosphorylation and inhibitory neurotransmission. RESULTS: Compared with controls, 488 transcripts were decreased and 67 were increased (p < 0.05, 1.5-fold) in the MS cortex. Twenty-six nuclear-encoded mitochondrial genes and the functional activities of mitochondrial respiratory chain complexes I and III were decreased in the MS motor cortex. Reduced mitochondrial gene expression was specific for neurons. In addition, pre-synaptic and postsynaptic components of GABAergic neurotransmission and the density of inhibitory interneuron processes also were decreased in the MS cortex. INTERPRETATION: Our data supports a mechanism whereby reduced ATP production in demyelinated segments of upper motor neuron axons impacts ion homeostasis, induces Ca2+-mediated axonal degeneration, and contributes to progressive neurological disability in MS patients. Ann Neurol 2006.
PMID: 16392116 [PubMed - as supplied by publisher]
I wish that it was easier to explain in layman's terms, but the other links I posted above and Robin's explanation are about the best that I can do.
Mitochondria is what feeds a cell energy:
"Mitochondria are sometimes described as "cellular power plants", because their primary function is to convert organic materials into energy in the form of ATP..."
ATP is what stores and transfers the energy within the cell itself:
"Adenosine 5'-triphosphate (ATP) is the nucleotide known in biochemistry as the "molecular currency" of intracellular energy transfer; that is, ATP is able to store and transport chemical energy within cells. "
The ions and the functioning of the ion channels is what moves that energy out of one cell to another (thereby transferring the messages from the brain to other parts of the body).
The CNS is sort of like a huge electrical wiring harness in a car. All of these terms relate to how the cellular "electricity" in the body is produced, transfered, converted, and then utilized (via ion channels) to and from the rest of the body via the axons (from one axon to the next). And it is a very precise balance between the three ions to open and close the "gates" between cells and axons that allows the energy to "move" throughout the body.
Just like a car that has a "short circuit" somewhere, when any part of this process is interrupted or becomes dysfunctional for any reason, then cells and neurons die (apoptosis), axons degenerate, etc.
Anyway, as has been found in research, the axonal degeneration and eventual progression of disability in MS is caused by the dysfunction of the exchange of nerve signals through the axon. It's like an electrical wire has been cut. Even if an axon has been demyelinated, it can still work just fine (transfering nerve signals from the brain to other parts of the body), as long as it does not get bombarded with too much Ca2+ (ionic calcium influx), which is what causes the axon's eventual demise in MS.
Neuroprotection will basically involve protecting the axon from the influx of Ca2+. The influx of Ca2+ can also be affected via the manipulation of the potassium and sodium channels.
Does this help any?
Sorry I can't do better.
EDIT: Oh, and what they are saying in the above article is that they are finding additional and various physiological mechanisms that end up causing the Ca2+ influx.
Which then may lead to several methods or medications that work to prevent that.
SECOND EDIT: And you know, I just noticed this statement from the above abstract: "In addition, pre-synaptic and postsynaptic components of GABAergic neurotransmission and the density of inhibitory interneuron processes also were decreased in the MS cortex."
If anyone recalls the narrative I posted back in June, 2004 (which you can still find on this website), I questioned in it whether affecting GABA and the synapses wouldn't be beneficial in MS! I just realized that! Well, I'll be darned!
Ok..........I had to go look myself as to what I had speculated on in my very first attempt at research. In my June, 2004 article, I proposed:
...."The survival of oligodendrocytes is crucial to sustain or repair myelin in MS. Oligodendrocytes contain GABA. Levetiracetam exhibits effects and regulation of GABAa. Desipramine shows affects (secondary message) on GABAb. Might this combination not prove HIGHLY beneficial in MS, as it not only may affect the survival to maturity of oligodendrocytes, but this combination of medications appears to regulate ion channels -
maintains sodium density and reduces potassium? (Also see Dr. Peter Calabresi's recent theory on potassium channels and MS.) There is also evidence of desipramine’s beneficial effects on sulfatide, thereby exhibiting further indication of the drug’s assistance with the survival of oligodendrocytes." ....
Good heavens! I think I sometimes freak myself out!!