If you are able to hold a hand or leg, for example, it is very likely that you will be able to carry on a conversation. In other words, this test will help you determine whether or not ALS/ALSSP is curable. This protein is needed by a host of cells throughout the body to perform basic cellular functions, such as growth, reproduction, and immune function. But a genetic mutation in the gene has been found to cause the same genetic damage. When a person with Huntington's is exposed to a toxic concentration of glutamine in his bloodstream, the protein in the glutamine is degraded, releasing excess glutamate that interferes with the normal process through which cells of the brain produce nerve impulses and transmit them to other parts of the nervous system. It is this damage and ascorbic acid that leads to the onset of memory loss in the afflicted, and makes Huntington's seem not so much more likely than a heart attack.
The reason for this is not clear, but it would seem that glutamate is involved: if there is no glutamine, nothing else is produced. So, what causes it, and why is the disease so lethal? One of the most common theories on the cause of Huntington's is the notion of a neuroadaptive response, i.e. It may be that a person with Huntington's is so used to using up his glutamine that his body does not produce enough of it in the early stages of disease, or that he is genetically predisposed to a glutamine deficiency. Another possibility is that a deficiency of the vitamin B6 can lead to a reduced ability to metabolize glutamine, resulting in a toxic buildup of excess glutamate, which causes the disease. One way of understanding the nature of this disease is as follows.
In order to keep from dying in the first place, the body must constantly make use of its glutamine stores in order to produce more of these essential amino acids. In order to maintain adequate levels of these amino acids, the body must make large amounts of the substance called glutamine. When these amino acids are no longer available, the body must make some of its own. If this condition persists, the brain will not be able to function efficiently, and the symptoms of the disease become more severe. In the early stages of the disease, it is the increased production of excess glutamate that causes the body to die, and it is this excess glutamine that is responsible for this disease. In the late stage, when the disease has caused the body so much damage that the body no longer produces enough glutamines, the glutamine stores are depleted, and the body will begin to die.
As such, the disease is not a ascorbic acid condition; it is rather a chronic state of chronic disease. DNA, and as this is not normally produced when a person has the disease, the excess glutamate that is released from this gene leads to a protein abnormality. The gene's deletion results in a protein with a different amino acid sequence, but the body cannot make this protein. It is this protein that is responsible for the death of the body's cells.