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Gene Behind Lincoln’s Diseas

ong, wire-like extensions that connect nerve cells. The worms suffered increasing paralysis, and then died.

"It's incredible and so very simple that this one protein is what keeps neurons from breaking in your body," Bastiani says. "The entire functioning of the nervous system depends on these wire-like axons between nerve cells."

Jorgensen says the mutant gene also may be involved in other neurodegenerative diseases and in brain damage that results from stroke or sports injuries.

"In the late stages of a variety of neurodegenerative diseases, you get irreversible nerve cell loss, and it's possible that is due to loss of this springy protein and nerve elasticity," says study co-author Marc Hammarlund, a University of Utah postdoctoral researcher in biology and HHMI research associate.

That means protecting spectrin in nerve cells potentially could serve as a treatment to slow progression of some neurodegenerative diseases, he adds.

Last year, University of Minnesota researchers reported they examined 299 living descendants of the Lincoln family and found the mutant beta spectrin gene in 125 of them, and 90 already had symptoms of what family members call "Lincoln's disease."

Those researchers reported there was a one-in-four chance the 16th president had spinocerebellar ataxia type 5. They cited a journalist's 1861 description of the tall, lanky Lincoln's "shambling, loose, irregular, almost unsteady gait."

Jorgensen says Lincoln who was born in 1809 and became president in 1861 may have had early-stage SCA5 that had not progressed much by the time he was assassinated in 1865 at age 56.

Most of a nerve cell's length is the thin, wire-like axon. A typical axon's diameter is about 5 microns in humans, or one-twentieth the thickness of a human hair. Every movement we make "puts stress on neurons," Bastiani says. Yet the thin axons do not break.

In the new study,
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