Decreased glutamate transport by the brain and spinal cord in amyotrophic lateral sclerosis

Article Abstract:

Decreased clearance of the neurotransmitter glutamate may cause neurotoxicity in patients with amyotrophic lateral sclerosis (ALS). ALS is a progressive disease of unknown cause that causes degeneration of nerve cells. Transport of glutamate was measured in nerve tissue obtained after death from 13 ALS patients, 15 patients with Alzheimer's disease, 12 patients with Huntington's disease and 17 healthy individuals. In ALS patients, transport of glutamate was 59% lower in the spinal cord, 70% lower in the motor cortex, and 39% lower in the somatosensory cortex, compared with healthy individuals. Glutamate transport was normal in other types of nerve tissue in ALS patients. No abnormalities in glutamate transport were found in patients with Alzheimer's disease or Huntington's disease, compared to healthy individuals. Transport of gamma-aminobutyric acid and phenylalanine were normal in motor cortex tissue from ALS patients, compared to healthy individuals. Glutamate is the main neurotransmitter in the brain, but higher concentrations can cause degeneration of nerve cells.

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Amyotrophic lateral sclerosis and glutamate - too much of a good thing?

Article Abstract:

Clearance of the amino acid glutamate may be reduced in patients with amyotrophic lateral sclerosis (ALS), a progressive disease that causes degeneration of nerve cells. Glutamate is a neurotransmitter, or signaling substance, found in the brain and spinal cord. Nerve cells are normally exposed to only low levels of glutamate, but certain diseases cause reduced uptake or increased release of glutamate. Overexposure to glutamate and similar substances can cause cell damage and death, or excitotoxicity. A research study found that uptake of glutamate by nerve cells was lower in the spinal cord or in parts of the brain tissue from ALS patients. This finding contributes to understanding the underlying mechanism for excitotoxicity. Drugs have been developed that block excitotoxicity caused by other neurotransmitters in patients with acute illnesses. Developing a drug to block excitotoxicity in patients with a chronic disease such as ALS would be more difficult. An alternative would be to develop a drug that prevents injury to nerve cells from excitotoxicity.

Editorial

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Serum antibodies to L-type calcium channels in patients with amyotrophic lateral sclerosis

Article Abstract:

The presence of antibodies against L-type voltage-gated calcium channels (VGCC) in patients with amyotrophic lateral sclerosis indicates that autoimmunity may be a factor in this disease. Amyotrophic lateral sclerosis, also known as Lou Gehrig disease, is a degeneration of the nervous system resulting in weakness, paralysis and eventually death. Proper regulation of calcium channels is important to the function of the nervous system. Blood samples from 48 patients with amyotrophic lateral sclerosis were compared with samples from patients with other types of neural and autoimmune diseases and with those from normal subjects. Antibodies to L-type VGCC were found in 36 patients with amyotrophic lateral sclerosis, one out of 25 normal patients and one out of 35 patients with other types of neurologic diseases. Furthermore, the number of antibodies seen increased with progression of the disease. These findings call for additional studies on the role of autoimmune mechanisms in this disease.

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