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Surprise-surprise
Medical Research is finally catching up to my patent
written in 1996 where I showed the connection between autoimmune disorders,
decreased ATP production, and toxins.
Cause
Of Nerve Fiber Damage In Multiple Sclerosis Identified
-Decreased ATP production may be a factor!
Researchers
have identified how the body’s own immune system contributes to the nerve
fiber damage caused by multiple sclerosis, a finding that can potentially aid
earlier diagnosis and improved treatment for this chronic disease.
The
study reveals how immune system B-cells damage axons during MS attacks by
inhibiting energy production in these nerve fiber cells, ultimately causing them
to degenerate and die. Study results appear in the Oct. 15 issue of the Journal
of Immunology.
B-cell-axon
activity is an emerging area of MS research, one that is changing how scientists
and clinicians can look at this disease. In this study, Dr. Yufen Qin and fellow
researchers from UC Irvine’s
School
of
Medicine
analyzed spinal fluid and tissue samples from MS patients to identify
substances that stimulate a B-cell immune response. They noted an increased
level of B-cell antibodies on lesions and in spinal fluid bound to two specific
enzymes – GAPDH and TPI.
These
two enzymes are essential for efficient energy production. The researchers
believe that the binding of these antibodies to these enzymes – GAPDH, in
particular – may lower the amounts of ATP
– the chemical fuel for cells – available in cells, which eventually can
lead to axon cell degeneration
and death. In addition to the energy-production function, GAPDH is involved with
a number of genetic activities, such as RNA translocation, DNA replication and
DNA repair.
Other
recent studies have shown that binding of inhibitors to GAPDH and TPI causes decreased
ATP production in neurons, followed by
progressive neuronal degeneration and death. Moreover, patients with TPI
deficiency can develop progressive neurological disorders.
“This
research is exciting and potentially important for future treatments because it
identifies new antibodies associated with MS that can be targeted with emerging
therapies,” said Qin, an assistant professor of neurology. “Significantly,
these are the first antibodies to be identified with axon activity, which is a
new area researchers are exploring in the pathology of MS.”
MS
is a chronic central nervous system disease that can cause blurred vision, poor
coordination, slurred speech, numbness, acute fatigue and, in its most extreme
form, blindness and paralysis. Some 400,000 Americans have this disease. Its
causes are unknown, and symptoms are unpredictable and vary greatly in severity.
Much
MS research is focused on an autoimmune process in which T-cells attack and
damage myelin, the fatty insulating tissue of axons. These T-cells do not attack
axons themselves; the process of demyelination interrupts electrical impulses
that run through these nerve fibers, thus causing MS symptoms. Demyelination has
been considered the central feature of MS.
Recently,
however, Qin has been among a group of researchers who have discovered that
B-cells too are involved with the autoimmune response to MS. Instead of
targeting myelin, these B-cells attack axons directly. Axons are the long,
slender fibers of a neuron that serve as the primary transmission lines of the
nervous system, and as bundles they help make up nerves.
Research
at UCI and elsewhere has shown that myelin grows back if the T-cell autoimmune
response is turned off, and drugs exist or are in development to block
demyelination. Axons, in turn, repair very slowly, which implies that B-cell
attacks on axons may have a significant impact on the chronic central nervous
system damage caused by MS.
“Since
this area of research is in its early stage, it’s important to understand the
process by which these B-cell responses happen,” Qin said. “Hopefully, by
identifying these two crucial enzymes, it will lead to a greater understanding
of MS and lead to more effective treatments for people who live with this
disease.”
Johanna
Kolln, Hui-Min Ren, Reng-Rong Da, Yiping Zhang, Dr. Michael Olek, Dr. Neal
Hermanowicz, Lutz G. Hilgenberg, Martin A. Smith and Dr. Stanley van den Noort
of UCI and Edzard Spillner of the
University
of
Hamburg
also worked on the study. The National Multiple Sclerosis Society and the
National Institutes of Health provided funding support.
http://www.sciencedaily.com/releases/2006/10/061017084642.htm
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