Get ready for this one.  It's a doozy.

After a decade of research into A-beta as the enemy in Alzheimer's Disease--

A molecule widely assailed as the chief culprit in Alzheimer's disease unexpectedly reverses paralysis and inflammation in several distinct animal models of a different disorder — multiple sclerosis, Stanford University School of Medicine researchers have found.

This surprising discovery, which will be reported in a study to be published online Aug. 1 as the cover feature in Science Translational Medicine, comes on the heels of the recent failure of a large-scale clinical trial aimed at slowing the progression of Alzheimer's disease by attempting to clear the much-maligned molecule, known as A-beta, from Alzheimer's patients' bloodstreams. While the findings are not necessarily applicable to the study of A-beta's role in the pathology of that disease, they may point to promising new avenues of treatment for multiple sclerosis.

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Dr. Lawrence Steinman of Stanford  (the inventor of Tysabri who warned you not to take it) has now discovered that A-beta treats EAE.  Yup.  Mice that were injected with the protein that we believe creates Alzheimer's Disease have a reversal of MS.

Sophisticated laboratory tests showed that A-beta countered not only visible symptoms such as paralysis, but also the increase in certain inflammatory molecules that characterizes multiple-sclerosis flare-ups. "This is the first time A-beta has been shown to have anti-inflammatory properties," said Steinman.

Actually, it's been known for quite some time that A-Beta protein is a helpful and essential protein in normal brain function.

In a new study published this month in Nature Neuroscience, Dr. Slutsky finds that amyloid-beta is essential for normal day-to-day information transfer through nerve cell networks in the brain. "If this protein is removed from the brain," says Dr. Slutsky, "as some drugs in development attempt to do, it may cause an impairment of neuronal function, as well as a further and faster accumulation of amyloid-beta in Alzheimer's."

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This situation reminds me of the "double think" from the Ministry of Information in the novel 1984-- language which deliberately disguises, distorts and reverses the meanings of words to keep the masses in a perpetual state of unknowing.

A-beta is evil!  A-beta is good!  The war is with Eurasia!

Medical research has become so convoluted, it seems impossible to follow.  And that makes it easier to sell us drugs.

Could it be that the target of the pharmaceutical therapies for Alzheimer's Disease may actually be an essential protein?  And blocking A-beta is harmful, rather than helpful?  Is this why all of the Alzheimer's drugs which block beta amyloid protein fail to stop Alzheimer's from progressing?

Doesn't this remind you of the recent news that beta interferon fails to stop progression in MS, even though it mutes the immune system?  It should stop MS progression, but it doesn't.

link to Marie's note on The Interferon Problem

Here's the elephant in the room question which no one is asking. What if the brain's reaction in Alzheimer's and MS is an over-reaching, yet natural healing response to injury?  What if the brain is responding to hypoperfusion, slowed cerebral bloodflow, hypoxia, and the inflammatory cascade?  And depending on your genetic predisposition and age, you may develop MS, Parkinson's or Alzheimer's as a response to this injury?

which is why this new drug targets inflammation in all these diseases

Dr. Paula Grammas has been studying this for over a decade....she has incredible data, but can't get funding.

link to Dr. Grammas' research into Alzheimer's disease pathogenesis related to the vasculature

Stys and colleagues propose a similar degenerative aetiology for MS, Alzheimer's, Parkinson's and dementia-with reactions associated with the age of onset.

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Maybe Dr. Steinman could stop thinking about his own personal gain and drug development?  

"There probably is a multiple-sclerosis drug in all this somewhere down the line," he said.

Maybe, just maybe, Dr. Steinman could walk over to Dr. John Cooke's lab and talk to him about endothelial dysfunction, hypoperfusion and the animal model of CCSVI?  Maybe he could work with Dr. Cooke and Dr. Dake--colleagues at his university-- and help them.  Maybe he could provide neurological oversight to Dr. Dake's venoplasty trial?  

Joan