Are Plaques really "Brain Pearls?"

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Are Plaques really "Brain Pearls?"

Postby Ruthless67 » Sun Sep 05, 2010 11:45 am

In the September AARP Bulletin, Vol. 51 No. 7 there is an article titled, Alzheimer’s a New Theory.

The part I found very interesting was when they talked about plaques. Here are a couple of excerpts from the article.

Alzheimer’s disease is characterized by two main elements - the sticky plaques that form outside the brain cells, and tangles of another protein, tau, that twist around the inside of the cells. Both are thought to play a role in the progression of the disease.

The plaques and oligomers are originally formed from a protein found in the body. This amyloid protein breaks down naturally throughout our lives.

Tanzi and others suspect that as the body ages, too many of these protein clumps create a damaging buildup in the brain. They also may trigger the creation of tau tangles that further gum up the brain’s signaling system.

The brain may try to remove the offending oligomers by forming plaques. Tanzi goes so far as to call the much-vilified plaques as “brain pearls”. He says that just as an oyster creates a pearl around a grain of sand to protect itself, plaques may serve as traps for the oligomers that are attacking the brain.

Researchers have found that some people who never had dementia nevertheless have brains inundated with plaques. It may be, they theorize, that their brains are exceptionally good at converting the offending “sand” into “pearls”.


I find the above article interesting, because some time ago I saved the below excerpts to refer to and they seem to me to be related. Am I way off base here?

Changes in normal appearing white matter in multiple sclerosis are characteristic of neuroprotective mechanisms against hypoxic insult. I have been supposing for a while that the fibrin/scars/lesions are a protective mechanism more than a "normal" scarring - a protection from further injury, rather than a reaction to an injury. http://tinyurl.com/mark-abstract.

Some time back, Marcstck (Marc) wrote:
Rusty Bromely, the COO of The Myelin Repair Foundation, was open to the notion of CCSVI. Rusty had an interesting take on the matter of iron deposition, saying that he didn't think it was being deposited by the reflux of blood itself. He believed that if CCSVI was indeed responsible for the iron deposition being found in MS brains, it was because the reflux of deoxygenated blood was leading to the death of oligodendrocytes, which in turn were releasing iron into the brain. Needless to say, I was blown away by the fact that he was so well-versed in the theory that he could make that distinction.

How does Multiple Sclerosis do it’s Damage? http://www.mult-sclerosis.org/howms.html

This article said “Oligodendrocyes belong to a larger grouping of maintenance cells called glial cells. Their importance has recently become better understood and, as more and more is discovered about MS, the more central oligodendrocytes, or more accurately their death, has become. In some ways, it is fair to say that multiple sclerosis is a disease of oligodendrocytes.”


So if we put the two statements together, Rusty’s & the article mentioned above, we get:

“Oligodendrocyes belong to a larger grouping of maintenance cells called glial cells. Their importance has recently become better understood and, as more and more is discovered about MS, the more central oligodendrocytes, or more accurately their death, has become, because, the reflux of deoxygenated blood in the CCSVI protocol leads to the death of oligodendrocytes, which in turn releases iron into the brain!!!!!!!!!”

So anyway which comes first, the egg or the chicken…..are plaques the villains or the pearls, lol.
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Postby ozarkcanoer » Sun Sep 05, 2010 12:28 pm

Hi Ruthless, I am glad to see you posting here again ! This is a little off of the topic, but related. What befuddles me about both the CCSVI hypothesis and the autoimmune hypothesis of MS is that when you get right down to the nuts and bolts of it all, i.e. just what is the initiator of the inflammatory attack on the brain ? and show me a nice computerized molecular biology movie or simulation that shows how attack progresses over time ?, well the CCSVI hypotheses has a handwaving model as does the autoimmune model. NOBODY really know the answers to these questions. So I find it odd that neurologists or any researcher for that matter would turn his nose up at the CCSVI model since the autoimmune model at this point is almost as empty. Yep, the immune system is involved but they don't seem to really know much more. I was encouraged to be educated by the NMSS when had my diagnosis. And what I found out is that they don't know much and the CRABS are iffy. Some NMSS guru should write an accessible book about what is currently known about MS and what is just "believed".

I know that there is a very smart researcher here at the Washington University School of Medicine who (probably using the EAE model) is trying to work out some of the signaling in the immune response.

I really wish I knew if ANYBODY is trying to create a mouse model of CCSVI !!!!!!!!!

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Postby Ruthless67 » Sun Sep 05, 2010 1:06 pm

I believe the Neurologist at Stanford (Dr.Freedman I think) was trying to get funding for a mouse model but didn't get funding.

I think I read that on another thread here at TIMS.

Lora
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Postby ozarkcanoer » Sun Sep 05, 2010 1:17 pm

I remember that too, Ruthless. But these researchers who work with mice daily should certainly be able to try to create CCSVI mouse model without a lot of $$$$. It is odd that there is so little talk about this. I think there was a Stanford researcher who Joan found who was going to try a mouse model. Last fall when I had a chance to talk with some really smart neuroscientists I was told that a CCSVI mouse model is certainly doable. They work with these poor little creatures daily on all sorts of research. Sounds much easier to me than double-blinded clinical trials of the procedure with sham surgeries on a large population of people with MS ?

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Postby Ruthless67 » Sun Sep 12, 2010 11:00 am

Ozarcanoer,

Did you see Cece's post about this particular rat study?

http://www.thisisms.com/ftopicp-133372-.html#133372

Lora
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More "Pearl's"

Postby Ruthless67 » Sun Sep 12, 2010 11:13 am

Study shows evidence that myelin-producing cells die before there is any immune system activity

March 18, 2004
Paul Jones
All About Multiple Sclerosis

http://www.mult-sclerosis.org/news/Mar2 ... eofMS.html

Michael Barnett and John Prineas of the Institute of Clinical Neurosciences at the University of Sydney, Australia, suggest that the first stage of the development of a new multiple sclerosis lesion is mass suicide of the oligodendrocytes over a relatively small area. Barnett and Prineas observed oligodendrocytes in which the central nucleus was shriveling up - a typical sign of a cell committing suicide. Other cells in the brain were also changing. Microglia, another type of maintenance cell which can swallow up dead and dying cells, were forming long extensions ready to engulf the dead and dying oligodendrocytes. (In other words Brain Pearls?) Additionally, a group of proteins, called complement, (Are these the amyloid proteins Dr. Gandy talks about?) which are responsible for activating the body's rubbish-collecting cells, had collected on the myelin. Crucially, the rubbish-collecting cells of the immune system, the macrophages, had not yet appeared in the lesion.
Within one or two days of lesion formation, all the oligodendrocytes had disappeared. The authors suggest that they had been swallowed up by the microglia. The spaces that they had once occupied were now full of liquid forming what is known as edema.


I keep running across research that all seem to point back to dying oligodendrocytes and the thought that it is their dying off that starts the ball rolling in the auto-immune response.

Such as the above article published in 2004. But this Idea of the lesions being “Brain Pearls” is new to me. Dr. Gandy’s research into Oligomers and Alzheimer’s that I quoted in my first post on this thread with the link below, was just written up.

Alzheimer: New Science Sheds Light on the Cause of Alzheimer’s Disease
<shortened url>

Just like Hubbard finding CCSVI in it’s first Parkinson’s patient, I think, in my humble and totally layperson’s opinion, that we might find more parallels in all these different classifications of diseases. It sure seems to me that there are similarities that need to be looked at.

That won’t be easy though, just look at the fight we are having with some sectors not wanting to give ground to another theory. Can you image all the disciplines’ trying to work together for a common goal, like a CURE.

Probably won’t happen, not when there is still a bundle of money to be made out of TREATMENT.
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Postby Cece » Sun Sep 12, 2010 11:14 am

Ruthless67 wrote:Ozarcanoer,

Did you see Cece's post about this particular rat study?

http://www.thisisms.com/ftopicp-133372-.html#133372

Lora

It's with a created AVM malformation, not a CCSVI malformation. But they were looking at the effects of chronic hypoperfusion, which is something we know we have as MSers; even the neurologists agree to that much.
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Postby Ruthless67 » Sun Sep 12, 2010 11:31 am

Here’s more of what Dr. Gandy and other’s in the article are saying,

Dillin, of the Salk Institute of California, started pursuing the same oligomer theory several years ago. Then the idea was so controversial, Dillin says, that some scientists would walk out of the room when he made his presentation at conferences. Now, he says, many of the top researchers in the field are convinced.

Dillin fears we may even discover that drugs designed to break down plaques may speed the disease’s progression.

“I think the plaques are a sign that your brain was trying to do something very beneficial for itself in the last stages of the disease,” Dillin says. “If you go in and take these plaques apart, you’re going to make oligomers, and that could actually be worse.”

Then, in 2004, scientists described mice that had no plaque but nevertheless showed signs of dementia. Other scientists showed that injecting rats with the oligomers caused memory loss. Another lab conducted an experiment to turn oligomers into plaques—they’re made of the same protein—and “when they did this gene trick, the mice got better, their memory improved,” Gandy says.


So, anyway, I find it fascinating. If plaques/lesions are brain pearls and not so much our enemy, but the attempt to protect the brain from further attacks, then to me that’s one more feather for Venous research into the CCSVI theory.

Now having said my peace, I'll let this thread die of natural causes, lol.
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Postby lyndacarol » Sun Sep 12, 2010 11:43 am

Ruthless67-- Your link to the article, Alzheimer: New Science Sheds Light on the Cause of Alzheimer’s Disease, would not work for me. I have no idea why not – I am relatively computer-illiterate.
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Postby Ruthless67 » Sun Sep 12, 2010 11:45 am

I just read this quote of Dr. McDonald’s in rebuttal to something Dr David Spence, a neurologist at U of Western Ontario, had to say about CCSVI. And found it interesting to my discussion above.

I think Neurology is stuck “IN THE BOX along with the IMMUNE THEORY”

Sandy McDonald, RVT, MD, FRSCS, FACS Vascular Surgeon Medical Director, Barrie Vascular Imaging 50 Alliance Blvd.

"Modern neurology holds that MS is an autoimmune, inflammatory syndrome of unknown cause, revolving around that model. What if they're wrong? It may be that nobody finds a cure for M.S. because nobody thinks outside the box."



Ok, now the thread can die, lol
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Postby Ruthless67 » Sun Sep 12, 2010 12:58 pm

Lyndacarol,

Sorry about that, try this one.

http://www.aarp.org/health/conditions-t ... sease.html

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