Pretty interesting....although not investigated in humans yet:

http://ms.about.com/b/2009/06/02/ms-...yelin.htm?nl=1

Here is some info from dead MS folks that shows LOTS of "other than myelin" damage.

jackD


"1: N Engl J Med. 1998 Jan 29;338(5):278-85.

Comment in:
N Engl J Med. 1998 Jan 29;338(5):323-5.

Axonal transection in the lesions of multiple sclerosis.

Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mork S, Bo L.

Department of Neurosciences, Lerner Research Institute, Cleveland Clinic
Foundation, OH 44195, USA.

BACKGROUND: Multiple sclerosis is an inflammatory demyelinating disease of the
central nervous system and is the most common cause of neurologic disability in
young adults. Despite antiinflammatory or immunosuppressive therapy, most
patients have progressive neurologic deterioration that may reflect axonal loss.
We conducted pathological studies of brain tissues to define the changes in
axons in patients with multiple sclerosis.

METHODS:
Brain tissue was obtained at autopsy from 11 patients with multiple sclerosis and 4 subjects without brain disease. Fourteen active multiple-sclerosis lesions, 33 chronic active lesions,
and samples of normal-appearing white matter were examined for demyelination,
inflammation, and axonal pathologic changes by immunohistochemistry and confocal
microscopy. Axonal transection, identified by the presence of terminal axonal
ovoids, was detected in all 47 lesions and quantified in 18 lesions. RESULTS:
Transected axons were a consistent feature of the lesions of multiple sclerosis,
and their frequency was related to the degree of inflammation within the lesion.

The number of transected axons per cubic millimeter of tissue averaged 11,236 in
active lesions, 3138 at the hypocellular edges of chronic active lesions, 875 in
the hypocellular centers of chronic active lesions, and less than 1 in
normal-appearing white matter from the control brains.

CONCLUSIONS: Transected
axons are common in the lesions of multiple sclerosis, and axonal transection
may be the pathologic correlate of the irreversible neurologic impairment in
this disease.

PMID: 9445407 [PubMed - indexed for MEDLINE]"

Well, I must say, this is not very uplifting news...
Do the DMDs only work on myelin-affected areas, or do they help stop progression in gray matter as well?

Thanks for this. I just giggled when I saw the autopsy revealed "active" lesions...pffft....too funny when they word things like that.

Really!! If they're "active" during an autopsy what on earth are they considered beforehand!?

I have NO HUMOR for you but I do have some more info..

PANIC!!! PANIC!! PANIC!!

MS is a TWO STAGE DISEASE!!!

1st is THE INFLAMMATORY Stage - Standard DMD work well here.

2nd is the NEURODEGENERATIVE PHASE The Standard DMD is weak and mostly unknown. However LDN may be effective for this stage of MS. In classic MS you have about 10 years of R/R MS followed by the next, 2nd phase which severly reduces mobility and loss of leg strength. Treatment with DMD during R/R stage could delay or hopefully avoid this stage.

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

http://home.ix.netcom.com/~jdalton/two%20stage%20MS.jpg


jackD

P.S. Look a the pic and guess what needs to be reduced or blocked. Hint it begins with the letter "g".

Incredibly timely given my doctor's appointment today regarding my new "black hole" lesion. I'm beat but I'm going to address this more when I further update that thread. I believe this is probably correct. But although obviously not good news, not necessarily as bleak as it sounds -- remember that depending upon where the damage is, the brain can be remarkable in re-routing itself to compensate (neuroplasticity). Many MS folks with even axonal damage are asymptomatic.

You are right about the brains ability to reroute itself BUT that compensatation ability does not work well in the spine.

So the 2nd stage of MS where the axons are attacked can cause some serious damage for which the body cannot compensate and the net effect is loss of lower limb strength.

jackD

Interesting to note that Glutamate attacks BOTH axons and myelin cells.

jackD


Neural Transm Suppl. 2000;(60):375-85. Related Articles, L

Glutamate excitotoxicity--a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis?

Werner P, Pitt D, Raine CS.

Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.


Glutamate excitotoxicity mediated by the AMPA/kainate-type of glutamate receptors is known not only to damage neurons but also the myelin-producing cell of the central nervous system (CNS), the oligodendrocyte.

In Multiple Sclerosis (MS), myelin, oligodendrocytes and axons are lost or damaged as a result of an inflammatory attack on the CNS. Activated immune cells produce glutamate in large quantities by deamidating glutamine via glutaminase.

Thus, we hypothesized that during inflammation in MS, glutamate excitotoxicity may contribute to the lesion. This was addressed by treating mice sensitized to develop acute experimental autoimmune encephalomyelitis (EAE) with an AMPA/kainate antagonist, NBQX.

Treatment resulted in substantial amelioration of disease, increased oligodendrocyte survival and reduced axonal damage, as indicated by the levels of dephosphorylated neurofilament-H. Despite the clinical differences, NBQX-treatment had no effect on lesion size and did not reduce the degree of CNS inflammation. In addition, NBQX did not alter the proliferative activity of antigen-primed T cells in vitro, further indicating a lack of effect at the level of the immune system.

In separate studies, infiltrating immune cells present in perivascular cuffs, commonly the site of entry for invading immune cells, were found to express glutaminase in abundance, supporting the production of glutamate in inflammatory lesions.

Thus, glutamate excitotoxicity appears to be an important mechanism in autoimmune demyelination and its prevention with AMPA/kainate antagonists may prove to be an effective therapy for MS.

PMID: 11205156 [PubMed]

From what you have researched, does glutamate appear to be the main culprit in nerve damage? If so, people really need to stop eating anything that contains MSG.

If one googles MSG, there are tons of places which list foods that always or usually contain this ingredient. I know that I get tremendous headaches after ingesting the stuff.

gmi