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        AlphaB-crystallin,drug reverses MS
                                All Natural treatments for all diseases please read this link  

              

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Jun 14 2007, 11:54 AM EST

GEN News Highlights

alphaB-crystallin, a protein found primarily in the lens of the eye, can reverse paralysis when injected in a mouse model of multiple sclerosis (MS), researchers at the Stanford University School of Medicine report.

alphaB-crystallin is not normally found in the brain but develops in response to the injuries inflicted on nerve cells by multiple sclerosis. For reasons not yet understood, the immune system considers the expression of the alphaB-crystallin protein in the brain a danger signal and attacks this healing substance.

"Like a runaway truck careening down a mountain and then having the brakes fall off, the immune attack against alphaB-crystallin worsens the situation," says Lawrence Steinman, M.D., professor of neurology and neurological sciences. And remarkably, he notes, addition of that protein works like restoring the failing brakes, returning control.

When they gave injections of the protein to mice with the equivalent of MS, their paralysis was reversed. The protein restored order by suppressing the cellular processes causing the damage. Dr. Steinman speculated that the mechanism is tolerization, similar to the process used in allergy shots when a person with an allergy gets an injection of the protein that is causing problems for the body so it can learn to ignore it.

Once the researchers had a grasp of what was occurring in mice, they turned to humans. Using a collection of spinal fluid samples, Dr. Steinman's team tested them on their antibody arrays. They found that the highest antibody response was directed against alphaB-crystallin, leading the researchers to speculate that the protein could possibly reverse the damage in humans as it does in mice.

Their findings were published in the June 13 advance online edition of Nature.

If you can use your brain you can do  this treatment at home today. Not from your eye but by eating a fish eye. Go buy fish, sushi is even better. What about a cow or goat eye

Not only the paralysis will reverse the disease will come to a halt for more on this read our flame within e-book a complete guide to natural treatments of all diseases. Follow the links below if you want to learn about current cause and natural treatments of MS.

Various different cell types have a role in the pathogenesis of multiple sclerosis. T cells express alpha4beta1 integrin (also known as VLA4), which allows them to bind to the ligands vascular cell adhesion molecule 1 (VCAM1) and osteopontin on the endothelial cells that line the venule. The T cells then undergo diapedesis and traverse through the perivascular cuff and travel through the extracellular matrix before gaining entry to the central nervous system (CNS) (a). Inside the brain, the secretion of cytokines, osteopontin and other molecules by T cells and antigen-presenting cells (APCs) damages oligodendrocytes, which produce myelin (b). Plasma cells produce myelin-specific antibodies that result in further damage to the myelin sheath (c). Surrounding the basement membrane of the venule are astrocytes that express alphaB crystallin, which can induce remission in experimental autoimmune encephalitis (EAE) (d). By contrast, blockade of alpha4beta1 integrin inhibits relapse in multiple sclerosis and, accordingly, osteopontin can induce relapse in EAE. IFNgamma, interferon-gamma; IL-23, interleukin-23.

In multiple sclerosis, the immune system launches an attack against the myelin sheath surrounding nerve cells, causing them to misfire. According to the Multiple Sclerosis Foundation, up to 500,000 people in the United States have been diagnosed with the condition, which causes varying symptoms depending on the location and extent of the scarring of the myelin sheath. Common symptoms include fatigue, weakness, vertigo, numbness and vision problems.

For reasons not yet understood, the immune system considers the expression of the alphaB-crystallin protein in the brain a danger signal and attacks this healing substance. "Like a runaway truck careening down a mountain and then having the brakes fall off, the immune attack against alphaB-crystallin worsens the situation," said Steinman. And remarkably, he noted, addition of that protein works like restoring the failing brakes, returning control.

If the same recovery is seen in humans, the protein might someday be used to treat multiple sclerosis. "It is a real delight to see that the same material that is naturally produced, that has these protective effects, could potentially be harnessed and used as a therapeutic itself," said Steinman.

 

High prevalence of anti-alpha-crystallin antibodies in multiple sclerosis: correlation with severity and activity of disease.

Agius MA, Kirvan CA, Schafer AL, Gudipati E, Zhu S.

Source

University of California at Davis, 95616, USA.

Abstract

INTRODUCTION:

The presence of T-cell reactivity to alphaB-crystallin in patients with multiple sclerosis (MS) has suggested that this small molecular weight heat shock protein (Hsp) may be an autoantigen in MS.

MATERIAL AND METHODS:

We have tested the serum of patients with clinically definite MS (n=30), other inflammatory neurological disease (n=22), non-inflammatory neurological disease (n=42) and healthy individuals (n=23) for systemic humoral responses to bovine alphaB-crystallin, to the homologous chaperone protein, alphaA-crystallin, and to another small Hsp, Hsp 27.

RESULTS:

Sixty-three percent of MS patients exhibited immunoreactivity to alpha-crystallin and this was present in all 4 of 4 non-ambulatory patients with MS. In contrast, serum concentrations in MS patients of antibodies to the small Hsp, Hsp27, and to myelin basic protein were negligible (P<0.001). Serum anti-alpha-crystallin immune responses were detected in significantly lower percentages of patients with other inflammatory neurological diseases (32%, P<0.025), and with non-inflammatory neurological diseases (12%, P<0.001). None of the healthy control individuals showed anti-alpha-crystallin reactivity. The concentration of anti-alpha-crystallin antibodies in patients with MS correlated with severe disease (P<0.05) and with active disease (P<0.025).

CONCLUSION:

Our observations support the notion that anti-alpha-crystallin autoimmune responses may contribute to pathogenicity in MS and may represent a mechanism of how recurrent attacks of MS develop subsequent to an isolated demyelinating episode.

 

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