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Protein involved in longevity also slows nerve degeneration
The results of previous research suggested that the nerve cell may activate a self-destructive process in the process of axonal degeneration. In the current series of experiments, Jeffrey Milbrand MD and colleagues studied cells derived from a line of mice whose axonal degeneration following injury is delayed compared to normal mice. They concluded that an unidentified factor activated in the cell nucleus by nicotinamide adenine dinucleotide (NAD) was responsible for providing the protection against axonal degeneration. Because Sir2 proteins are known to be activated by NAD, the researchers investigated this possibility by administered a drug to the cells called Sirtinol that prevents the action of Sir2, and found that the neuroprotective effect disappeared. In addition, giving extra NAD to normal mouse nerve cells induced the protective effect, yet this was also blocked by the drug.
Further experimentation identified the Sir2 protein active in these cells as SIRT1.
To confirm the involvement of Sir2 in NAD-dependent axonal protection, resveratrol, a polyphenol that enhances Sir2 activity, was administered to neurons prior to injury, and was found to offer a degree of protection comparable to that provided by NAD.
Dr Milbrand, who is a professor of medicine at Washington University School of Medicine, commented, “It's becoming clear that nerve cell death in these disorders is often preceded by the degeneration and loss of axons, the branches of the cells that carry signals to the synapse. If this mechanism for delaying or preventing axonal degeneration after an injury proves to be something we can activate via genetic or pharmaceutical treatments, then we may be able to use it to delay or inhibit nerve cell death in neurodegenerative diseases."
Amyotrophic Lateral Sclerosis
ALS is a rapidly progressive neuromuscular disease caused by the destruction of nerve cells in the brain and spinal cord. This causes the loss of nervous control of voluntary muscles, resulting in the degeneration and atrophy of the muscles. Eventually the respiratory muscles are affected which leads to death from an inability to breathe.
The most common form of vitamin B12 is cyanocobalamin. While this form of vitamin B12 works well to prevent anemia, it is the methylcobalamin form that is required to maintain neurological health. The liver naturally converts a small amount of cyanocobalamin into methylcobalamin, but to regenerate neurons and the myelin sheath that protects axons and peripheral nerves, higher doses of methylcobalamin are necessary. There is no known toxicity at these doses.
L-cysteine is a conditionally essential amino acid, one of only three sulfur-containing amino acids, the others being taurine (which can be produced from L-cysteine) and L-methionine from which L-cysteine can be produced in the body by a multi-step process. Cysteine plays a role in the sulfation cycle, acting as a sulfur donor in phase II detoxification and as a methyl donor in the conversion of homocysteine to methionine. Cysteine also helps synthesize glutathione, one of the body's most important natural detoxifiers. N-acetyl-cysteine is the acetylated form of L-cysteine, which is more efficiently absorbed and used.
The list of conditions that can be improved with N-acetylcysteine supplementation seems to grow each year. For example, N-acetylcysteine recently was shown to reduce the proliferation of certain cells lining the colon, and it may reduce the risk of colon cancer in people with recurrent polyps in the colon. N-acetylcysteine has been used in connection with chronic obstructive pulmonary disease, angina pectoris, gastritis, and heart attack (intravenously immediately following a myocardial infarction).
More recently, patients with other neurodegenerative conditions including amyotrophic lateral sclerosis, multiple sclerosis, diabetic neuropathy, and Alzheimer’s disease have been treated with N-acetylcysteine. These treatment outcomes indicate that if improvement in antioxidant status occurs, the potential exists for arresting progression of the disease and, in some cases, even improving the sufferer’s condition. N-acetylcysteine, with its proven safety and various antioxidant capabilities, may be a promising new tool in the treatment of such disorders.
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