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
4
1
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
B
crystallin, which can induce remission in experimental autoimmune
encephalitis (EAE) (d). By contrast, blockade
of
4
1
integrin inhibits relapse in multiple sclerosis and, accordingly,
osteopontin can induce relapse in EAE. IFN
,
interferon-
;
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.