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LEMS — Atchison

William Atchison (LEMS)
Using a mouse model of LEMS, Atchison will explore the means by which certain types of calcium channel proteins are recruited to compensate for the loss of other types of calcium channel proteins responsible for regulating the release of acetylcholine, the chemical messenger that carries signals between nerve cells and muscle.
Lambert-Eaton Myasthenic Syndrome (LEMS)

MDA awarded a research grant totaling $336,503 to William Atchison, professor of pharmacology/toxicology and acting dean for research at Michigan State University College of Veterinary Medicine in East Lansing. The funds will support Atchison's research into the biological mechanisms underlying Lambert-Eaton myasthenic syndrome (LEMS).

In LEMS, the immune system mistakenly mounts an attack, targeting proteins called "types P and Q calcium channels" located at the neuromuscular junction, the place where motor neurons (nerve cells) and muscles meet. These proteins regulate the release of acetylcholine, the chemical messenger that carries signals between the motor neuron and the muscle.

In previous MDA-supported work, Atchison found that mice treated with plasma taken from people with LEMS reacted to an attack on the P/Q calcium channels by recruiting members of other classes of calcium channels (types L and R) in an effort to compensate for loss of the P/Q types.

In his new work, Atchison plans to study the compensation strategy and determine how muscle-controlling nerve cells try to maintain their function via recruitment of the L and R types of calcium channels.

Atchison's work could pave the way to a gene therapy strategy based on increasing the availability of compensating proteins as a means of preventing disruption of the chemical messenger.

"MDA funding has been crucial in that it has allowed us to study a relatively rare neuromuscular disease, but one that has very severe consequences, and that affects the quality of life and its length in patients with LEMS," Atchison said. "It has also allowed us to focus on aspects of this disease that might help increase general understanding of how the neuromuscular system tries to compensate for damage in other forms of autoimmune disease."

Funding for this MDA grant began February 1, 2011.

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    • Volume 1, Issue 1, October 2011
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Grants at a Glance — Winter 2011

  • ALS — Barrett
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