Australian Study - AutoImmune Response May not Trigger MS

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Australian Study - AutoImmune Response May not Trigger MS

Postby seanthecaper » Sat Jan 30, 2010 10:32 am

From the UK MSRC a new study released on January 30 2010:

Australian study questions established concepts of early disease events in MS

Investigators at the University of Sydney have published a study suggesting that the earliest activity seen in the brain in MS is the destruction of cells that make myelin (oligodendrocytes), occurring before the onset of immune activity usually blamed for triggering the disease.

This provocative study, co-funded by many sources including the National MS Society, opens up new possibilities for finding the cause of the disease and developing new treatments. The study is authored by Drs. John W. Prineas, Andrew P.D. Henderson and colleagues, and is published in the December issue of Annals of Neurology (2009;66:739–753).

Background: Multiple sclerosis has long been thought to be triggered by immune attacks in the brain and spinal cord, causing a spectrum of neurological symptoms. Extensive research has been underway to better understand what triggers the immune attacks and which immune cells are involved, and to better understand the damage to the central nervous system that occurs during the course of MS. In addition to studies of immune activity underlying what has been considered an autoimmune process, another important approach has centered on pathology studies involving microscopic explorations of MS lesions (damaged areas, also called plaques) in the brains of people with MS.

The lead author of the current study, John W. Prineas, MB, BS, FRCP, was the 2001 winner of the John Dystel Prize for MS Research, an award given jointly by the National MS Society and the American Academy of Neurology. He was recognized for being the investigator who first described how myelin, the substance that insulates nerve fibers, is broken down in MS, and he was the first to demonstrate that myelin repair occurs during the course of MS through the body’s natural repair processes.

Current Study: For this study, the team used brain specimens from 11 people who had died early in the course of their MS, and the team also used comparison specimens from people with other disorders including stroke. Some of the tests focused on subsets of specimens from seven people who had lesions showing active myelin destruction. To get a sense of immune cell activity in the brain and at what stage it was occurring, the team examined newly active and resolved lesions, as well as nearby blood vessels, surrounding areas showing some disease activity and surrounding areas that appeared normal, and areas that were farther away from the lesions of interest.

Results: In tissues surrounding newly forming lesions, the investigators found evidence of the loss of oligodendrocytes with an absence of immune T or B cells that would normally be held responsible for launching the immune attack against oligodendrocytes and the myelin they produce. These and other immune cells, including scavenger cells (macrophages and microglia), were more numerous in lesions and surrounding tissues at apparently later stages of destruction and sometimes in lesions that were in the process of repair. In specimens from two very early cases of clinical onset of disease, they found few immune cells within the lesions and no evidence of activation of scavenger cells.

These and other unexpected findings from this study led the investigators to propose that the early immune activity seen in active lesions is that of macrophages and microglia, whose job it is to clean up and remove damaged myelin.

They propose that lesion formation is caused by something other than destructive immune activity led by inflammatory cells against a component of myelin or oligodendrocytes.

Comment: This study is a significant addition to a small but growing body of evidence that highlights the question of what triggers MS and whether there is something other than, or in addition to, the immune attacks that lead to tissue damage in the brain and spinal cord of people with MS. Further research, which is ongoing by investigators around the world, should shed further light on this question and may offer novel treatment approaches.

Note: The availability of donor brain specimens was crucial to this and other studies focusing on disease pathology

Source: US National Multiple Sclerosis Society (30/01/10) January 30, 2010
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This points toward a trigger that is not autoimmune. I hope this research brings us some better treatments.

Sean
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Postby cinder21 » Sat Jan 30, 2010 10:53 am

i already posted that
22 yr old male located in the caribbean. Suffering with MS like symptoms from early 2008 with multiple relapses under my belt with optic neuritis. Not dx'd as yet however. Hope is to ultimately be tested for CCSVI
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Postby seanthecaper » Sat Jan 30, 2010 1:45 pm

sorry for the repeat on the post

I'm just happy to see researchers looking at other factors other than autoimmunity.
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Postby cinder21 » Sat Jan 30, 2010 3:34 pm

same here
22 yr old male located in the caribbean. Suffering with MS like symptoms from early 2008 with multiple relapses under my belt with optic neuritis. Not dx'd as yet however. Hope is to ultimately be tested for CCSVI
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Postby avantitech » Sat Jan 30, 2010 5:18 pm

Folks,

In reference to the early phase of MS attacks the significance of this artice should not be underestimated as it clearly indicates that:

1. MS lesions occur initially as an adaptive immune response to tissue damage (which is good and normal as it is the dying tissue cells clean up stage);

and that

2. The tissue damage appears to be ischemic in nature.
In the wiki lookup for "ichemic" under 'mechanism' the following is noted:

"Ischemia can also be described as an inadequate flow of blood to a part of the body, caused by constriction or blockage of the blood vessels supplying it."

Of course it also shows that as the lesions grow in size and age a new subset of active immune cells are involved and it is postulated that this is the stage when long-standing autoimmunity response is imparted.

The plot thickens does it not?
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Postby shye » Sat Jan 30, 2010 7:11 pm

Avantitech,
No, actually it thins; clearly, with the info in the above post seen in light of the CCSVI theory we get closer to an answer.

And Seanthecaper,
I missed the earlier posting of this, and am grateful to see it now.
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Postby avantitech » Sat Jan 30, 2010 7:52 pm

Shye, we are agreed - the (CCSVI Story) Plot thickens as in:

This study provides more information to researchers and the Evidence is mounting in support of the CCSVI concepts.

as opposed to a "thin plot" of insufficient evidence.
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