This Is MS Multiple Sclerosis Community: Knowledge & Support

Hi,

I think that the problem may be in the mitochondria of oligodendrocytes. These organules in these cells are responsable of myelinization of neurons and important in the beta-oxidation of lipids. Myelin is 70% lipids!!!!
One important sustrate for the mitochondria is the oxigen. In case of hypoxia (CCSVI) the mitochondria is altered and induce the apoptosis of the oligodendrocytes. Also these phenomena could be increased if others factors like Metals (thimerosal, aluminium, etc) that are accumulated in the mitochondria of these cells.
The fatiga is a real symptom of mitochondria mal-function (see in the chronic fatiga syndrome).

Sorry for my english,

Moni.

Interesting post, I've been of the opinion for a long time that if we can figure out exactly why the oligodendrocytes are dying we will have a big piece of the puzzle figured out. Check out this thread from a while back looking at it from the iron overload aspect

http://www.thisisms.com/ftopict-11268-o ... ocyte.html

This seems like one of those obvious connections that is only obvious now in hindsight (with the CCSVI connection now known).

The mitochondria are suspected in chronic fatigue syndrome?

Dr Wahl, who wrote Up From the Chair documenting her dietary plus approach to recovering from ms has also written a book called Minding My Mitochondria. I think the puzzle pieces are starting to come together.

For those of you who slept through your science classes the Mitochondria are the "power plants" of the cells. Some have 1, some have many.

The mitochondria uses fuel to power whatever the cell does. It makes energy called ATP.

All cells have a job.....and some need a lot of energy to work some need very little.

Examples are :

Skin cells : need very little energy, they work but their energy needs are rather low.

Heart cells: these guys are workhorses they need lots of ATP production so they need lots of fuel ( oxygen, glucose, etc)

Brain cells( all types): these are the ATP HOGS, the brain cells need lots of ATP to make sure we can "think" and all the "automatic" functions can occur.
The brain uses 70% of your glucose and 35% of your oxygen-


In CCSVI both the oxygen and the glucose levels in the brain are less than normal.

It would be like being in a sealed room with a odorless toxic paint . It would make you very tired (fatigue), unable to think clearly, etc.

Damaged cells spill out their contents, thus the Oligoclonal bodies normally inside myelin cells are found outside them.

All brain mitochondria would be unable to meet their needs and they would eventually be damaged and then die.

_________________
Cat (Catherine Somerville on FB)
MegansMom
My 35 yo daughter is newly dx 8/19/10 (had 12 symptoms)
Dx with Type A CCSVI- 1 IJV & double "candy wrapper" appearance of her Azygos
Venoplasty done Sept 21, 2010
Doing extremely well-

Post venoplasty, can the cells recover from this? The oligoclonal bodies wouldn't get back in, even if the damaged cells are healing. Can the cells make more of these?

The way the mitochondria are constructed is so ingeneous, that can only be and in fact is the result of 2 Billion years of evolution. For the religious people among us, that can only be an act of God.

When the glucose is burned, there is an H+ that moves along the innerside of the cell tissue; in distinct steps. I think that it is precisely this H+ that restores the equilibrium of the ion pumps, i.e. that moves the K+ and Na+ along the outermembrane of the nerve cells to maintain a certain "charging" level.

It is this charge that can fire thousand of "potentials" that we need to transmit the signals from our brain to the muscles or in the other direction from our sensors back to the brain. If the ion pumps run down (because they lack glucose/oxygen), the charging/equilibrium of the ion pumps can not be maintained, the signals will not be transmitted anymore or at least be attenuated. And our motor functions stop or slow down..

See also e.g. http://www.thisisms.com/ftopic-15188-165.html

Yes Cece, in most cases the answer is sometimes.

Re-myelinatin occurs in other illnesses, so why not CCSVI? The Schwann cells are adaptable and will re-myelinate an adjacent axon if that axons Schwann cell died. Axons don't regenerate, but Schwann cells do. Axons are pretty tough too and not easily killed.

I have seen patients (when I was an ICU /CCU RN ) with post code or near
drowning hypoxic encephalopathy. Many patients improved. Not all but many.

I also saw a few with Guillian Barre syndrome a demyelinating disease that's caused by a virus. The patients were profoundly paralyzed but overtime they re-myelinated as long as they had good supportive care ( sometimes a ventilator) through the severe part of the illness.
Re-myelination occurs slowly but can occur. The recovering person must have adequate cerebral oxygen and cerebral glucose AND adequate WBCs to aid in the tissue repair and debris clean up.
Frequently GB patients are treated with IVIGg to boost the immune system in the rehab part of recovery. I think this is an "off label" use of IGg.

_________________
Cat (Catherine Somerville on FB)
MegansMom
My 35 yo daughter is newly dx 8/19/10 (had 12 symptoms)
Dx with Type A CCSVI- 1 IJV & double "candy wrapper" appearance of her Azygos
Venoplasty done Sept 21, 2010
Doing extremely well-

Mitochondria, apoptosis, iron overload, hypoxia, hypoglycemia, reflux, shear thinning, viscosity, red blood cell mechanics, age, genetics; it's such a complex problem it's no wonder there's no one-size-fits-all fix.

_________________
"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
'_MS' is over - if you want it
Patients sans/without patience

Hi all,
Thanks for the comments. I think that exist a lot of interest topics to continue thinking.
Now I was thinking that if the mitochondria of oligodendrocytes are affected, probably the CCSVI treatment + mitochondria treatments could help us more. I just to find this website:
http://www.umdf.org/site/c.otJVJ7MMIqE/b.5692887
Any experience?
Cheers,
Moni

Interesting paper:

Biochim Biophys Acta. 2011 May;1812(5):630-41. Epub 2011 Feb 2.

Analysis of the mitochondrial proteome in multiple sclerosis cortex.
Broadwater L, Pandit A, Clements R, Azzam S, Vadnal J, Sulak M, Yong VW, Freeman EJ, Gregory RB, McDonough J.
Source
Department of Chemistry and Biochemistry, Kent State University, Kent, OH 44242, USA.
Abstract
Mitochondrial dysfunction has been proposed to play a role in the neuropathology of multiple sclerosis (MS). Previously, we reported significant alterations in the transcription of nuclear-encoded electron transport chain genes in MS and confirmed translational alterations for components of Complexes I and III that resulted in reductions in their activity. To more thoroughly and efficiently elucidate potential alterations in the expression of mitochondrial and related proteins, we have characterized the mitochondrial proteome in postmortem MS and control cortex using Surface-Enhanced Laser Desorption Ionization Time of Flight Mass Spectrometry (SELDI-TOF-MS). Using principal component analysis (PCA) and hierarchical clustering techniques we were able to analyze the differential patterns of SELDI-TOF spectra to reveal clusters of peaks which distinguished MS from control samples. Four proteins in particular were responsible for distinguishing disease from control. Peptide fingerprint mapping unambiguously identified these differentially expressed proteins. Three proteins identified are involved in respiration including cytochrome c oxidase subunit 5b (COX5b), the brain specific isozyme of creatine kinase, and hemoglobin β-chain. The fourth protein identified was myelin basic protein (MBP). We then investigated whether these alterations were consistent in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS. We found that MBP was similarly altered in EAE but the respiratory proteins were not. These data indicate that while the EAE mouse model may mimic aspects of MS neuropathology which result from inflammatory demyelinating events, there is another distinct mechanism involved in mitochondrial dysfunction in gray matter in MS which is not modeled in EAE.


http://www.ncbi.nlm.nih.gov/pubmed/21295140

very interesting!

It's interesting when it says not to fast. I do better when I eat every two hours or so.

In all eucaryotic cells, the mitochondria organelles are responsible for generating energy in the form of ATP for the running of cell function. Part of the generation of ATP is to create an ion gradient across the wall of the mitochondrial organelle. This ion gradient is used to produce ATP from ADP and P+ (phosphorus). If there were something wrong with the biochemistry of mitochondria then perhaps not enough ATP energy would be produced. With a lack of energy a cell would be in trouble, maybe die.

ozarkcanoer

This is absolutely the point! But remember the brain cell mitochrondria fuels are not cut off, that is , the fuels -oxygen and glucose - are reduced, sort of an " intermittent starvation" . The brain might get adequate fuels some of the time ( dependent in the extent if the CCSVI and the number of blocked vessels and extent of % blockages and also patient position)and then inadequate at other times.
This may have a slow chronic damage effect as opposed to an acute insult and cell death. Slightly abnormal oxygen/glucose say for 16 hrs per day and then way subnormal for the other 8 hrs.

Also of significance , some areas of the brain- the Hippocampus ( memory) and Basal ganglia (smoothness of body motion) - are more easily effected by hypoxia than other parts. Although hypoxia in general will cause fatigue, headache and sleepiness, much like being overcome by a toxic fume or carbon monoxide-
If you look up anoxic or hypoxic encephalopathy (which is the extreme acute illness of hypoxia) and you think of a much less acute, Less severe but related effect this can explain a lot of the mood, psychological symptoms seen in MS.
Honestly this is probably the root cause of MS symptoms not the location of the classic MS lesions. Lesion location could never be matched to symptom.

_________________
Cat (Catherine Somerville on FB)
MegansMom
My 35 yo daughter is newly dx 8/19/10 (had 12 symptoms)
Dx with Type A CCSVI- 1 IJV & double "candy wrapper" appearance of her Azygos
Venoplasty done Sept 21, 2010
Doing extremely well-