Dr. Stys research

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Dr. Stys research

Postby Cece » Sat Apr 21, 2012 4:54 pm

Anyone know anything about Dr. Peter Stys? He presented at the Edmonton MS society meeting today, and says that "his research has shown that myelin dies from the inside out. One would expect, if MS were an autoimmune disease,the myelin would die from the outside in!" (Quoting Arlene Hubbard from the CCSVI in MS page.)

I am not sure what it means for myelin to be dying from the outside in, or the inside out! Is it that the myelin closest to the axon dies first, and other layers of myelin on top of it die next?
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Re: Dr. Stys research

Postby cheerleader » Sun Apr 22, 2012 10:42 am

Dr. Peter Stys is a stroke/ischemia injury researcher. Here is his paper on MS as a disease of axonal loss--
http://www.ohsu.edu/nod/documents/2007/ ... 202005.pdf

Stys received money from the MSSC to study progressive MS--
The Multiple Sclerosis Society of Canada and the Multiple Sclerosis Scientific Research Foundation announced a $3.8 million grant to investigate the complex interplay between degeneration and inflammation in multiple sclerosis (MS).

The grant will fund a study led by Dr. Peter Stys from the University of Calgary's Hotchkiss Brain Institute, which would investigate damage that occurs in MS prior to inflammation. This research may have special relevance for those with progressive forms of MS.


As far as the "inside out" comment--I think Arlene had it a bit confused. I believe that refers to the idea of gray matter injury preceding myelin degredation--
The inside/out-vs-outside/in terminology has been used in papers like this one:
http://www.springerlink.com/content/2kvdwd3gbljmlgf2/

This is the model Stys is using...that axonal degeneration and ischemic injury precedes myelin loss, or "inside-out" Which would explain why he "gets" CCSVI research, and didn't have as many objections to the research. He is primarily from the ischemic injury understanding of the science, as the first paper I linked shows....just the right person to bring into understanding the injury mechanism of CCSVI.
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Re: Dr. Stys research

Postby Dovechick » Sun Apr 22, 2012 1:21 pm

In short this means that CCSVI which may cause ischemia in the brain could lead to the death of tissues. He makes much to the auto-immune theory but we must remember that this was written in 2005, well before questions were being raised about the validity of the autoimmune theory.

From the Peter K. Stys paper: General mechanisms of axonal damage and its prevention.
Together, these data present evidence that mechanisms of injury to white matter in anoxia/ischemia and neuro-inflammatory diseases may be surprisingly similar, and neuro-protectants designed for ischemia may be effective adjuncts in neuro-inflammatory disorders such as MS.


Prineas and Barnett's research would support the Stys hypothesis.
Barnett and Prineas reported that in the post mortem examination of the brains of people who had died shortly after a relapse they discovered that the newly formed lesions showed signs of oligodendrocite apoptosis but no sign of immune activity. The changes showing in the oligodendrocite indicated damage by hypoxia, ischemia and excitotoxins. (Cregan et al. 2002)
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Re: Dr. Stys research

Postby Jason » Sun Apr 22, 2012 2:30 pm

The presentation in Edmonton was recorded and will be put online in a few days along with Dr. Hubbards presentation as he was there too.
Dr. Stys is a Stroke doctor that works out of Calgary, Alberta.
The MS Society of Canada gave him $3.8 million to continue his work.
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Re: Dr. Stys research

Postby Leonard » Tue Apr 24, 2012 2:08 am

They die because the nutrition / transcription process in the vessel walls fails.
The reason for that is that key receptors in vessel walls are weak and get blocked.
I am very serious about this: there is nothing wrong (=no genetic defect) with our astocytes/oligodendrocytes.
Because of receptor failing, there is a disconnect between the bloodstream (RBC carrying high ATP and the cells that lack ATP).
The diabetes relation in MS is known.
The first RR phase is because of (sleeping) bacteria, virusses etc.
The second SP/PP phase is caused by a connection of the porous gut and porous BBB, in combination with undernourished cells...
see also general-discussion-f1/topic15188.html, in particular the first posting on the first page and the last say 4 or 5 pages...
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Re: Dr. Stys research

Postby cheerleader » Tue Apr 24, 2012 9:22 am

Dr. Stys' research is very specifically looking at calcium overload and glutamate excitotoxicity due to damage in myelinated axons from ischemia and trauma. He's been working on calcium channel blockers, but understanding why there is ischemic injury in MS brains must be of interest to him, too. I think that's probably why he found the Hubbard's slowed perfusion study interesting.

I also think I understand the "inside/out" comment now....the axon, underneath the myelin, is what dies first...leading to the release of toxins, and degrading the myelin.

Dr. Stys is a neurologist/neuroscientist and a world leader in the detailed study of pathophysiological mechanisms of white matter injury in stroke and trauma. He has extensive expertise in electrophysiological recording methods in myelinated axons and his team has recently developed confocal, multiphoton and coherent anti-Stokes Raman scattering (CARS) imaging techniques for both fixed immunostained and live myelinated axons and glial cells.

Dr. Stys’ team discovered several novel injury mechanisms responsible for axo-glial damage in ischemia/trauma: Ca overload secondary to reverse Na-Ca exchange (Stys et al., J Neurosci, 1992) and glutamate excitotoxicty due to reversal of Na-dependent glutamate transport in damaged spinal axons (Li and Stys, J Neurosci, 1999). This endogenously released glutamate then activates newly discovered AMPA/kainate receptors on axons (Ouardouz et al., J Physiol, 2006), and surprisingly, NMDA receptors on oligodendrocytes and the myelin sheath itself (Micu et al., Nature, 2006). In addition, depolarization of damaged fibers leads to release of toxic amounts of Ca from intra-axonal Ca stores, dependent on L-type Ca channels and ryanodine receptors (Ouardouz et al., Neuron, 2003), via a mechanism very similar to excitation-contraction coupling in muscle cells. The various signaling molecules (glutamate receptors, Ca channels, nNOS, RyRs, and likely many others) are organized along the internodal axolemma under the myelin sheath in discrete “axonal nanocomplexes”, very reminiscent of arrangements at the post-synaptic membrane of conventional interneuronal synapses.

http://www.ucalgary.ca/spinalnerve/stys/
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Re: Dr. Stys research

Postby Cece » Tue Apr 24, 2012 12:07 pm

Yes, that makes sense, since the axon is inside the myelin, so you'd expect the myelin to die first if it was under external attack from the leukocytes, but if the axon is dying within the myelin, then that would indicate some other process is going on, such as ischemia or malnutrition.

You would also expect the nerve cells of the retina of the eye to be unaffected, since they are unmyelinated, if MS is a disease of the myelin, but they are in fact affected in MS and, as measured through OCT, are a better correlate to EDSS disability than MRI of the brain is.

Dr. Stys brings an excellent different point-of-view and knowledge base to the table. Understanding CCSVI is a multidisciplinary task, but treating CCSVI is in the hands of the IRs.
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