This Is MS Multiple Sclerosis Knowledge & Support Community

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”.

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.”

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.

Ruthless67 wrote:Ozarcanoer,

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

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

Lora

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.

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."