Genes and Cells in ALS

Researchers in Texas may have found the mechanism behind the progressive neurodegenerative condition amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease. The researchers say that a lack T cells, immune cells that help reduce inflammation, worsens the symptoms. Production of the cells is controlled by a gene called FoxP3; when the gene is inactive, the researchers found, the degeneration from the condition was more rapid.

ALS causes gradual diminishing of function as motor neuron cells in the spinal cord die off. The motor neurons are the medium through which the brain communicates with the muscles. The initial symptoms are weakness in the arms and legs, and difficulty in breathing and swallowing. Over time, the muscles atrophy and no longer work. There is not yet any known cure for the condition, which is estimated to affect about 15,500 Americans.

Medical research has established a link between inflammation and ALS, but that link is very complicated. Normally, inflammation is part of the process by which the body protects or heals from microbial invasion. It’s an important part of the healthy immune response. The death of motor neurons from ALS also seems to trigger inflammation, in the glial cells, but that inflammation seems in turn to worsen the effect on the motor neurons; the cells produce chemicals that damage the neurons surrounding them, damage that eventually destroys them.

While inflammation exacerbates disease in ALS patients, this inflammation is suppressed in some patients, said study author Jenny Henkel, a neurologist at Houston’s Methodist Neurological Institute, in a statement. “The data in our article suggest that regulatory T cells can suppress this inflammation.”

Another study, in Boston, found a type of cell in the blood that is associated with ALS. By looking for abnormal levels of these cells, called monocytes, doctors can detect ALS early and start treatment to slow its progression. Monoctyes also provide a line of investigation in the application of anti-inflammatory treatment to ALS.

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