Researchers have discovered the main culprit for nerve fibre damage in multiple sclerosis, which is triggered by the body's own immune system, which is vital for early diagnosis // and evolving improved treatment of a severe disease. The study indicated the manner in which immune system B-cells damage axons in the course of MS attacks by hampering the energy production in nerve fiber cells, ultimately bringing about natural death of these cells. Study is published 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. "Signific
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