http://www.msnbc.msn.com/id/16871414/


Lincoln had shattered nerves, study suggests
Disease would explain gangly walk president was famous for

By Heather Whipps

Updated: 12:42 p.m. ET Jan. 29, 2007

Abraham Lincoln may have suffered from a genetic disorder that literally
shattered his nerves, a new study on worms suggests.

http://www.msnbc.msn.com/id/16871414/


Lincoln had shattered nerves, study suggests
Disease would explain gangly walk president was famous for

By Heather Whipps

Updated: 12:42 p.m. ET Jan. 29, 2007

Abraham Lincoln may have suffered from a genetic disorder that literally
shattered his nerves, a new study on worms suggests.

Many of the president's descendants have a gene mutation that affects
the part of the brain controlling movement and coordination, researchers
discovered last year. The mutation prevents nerve cells from
"communicating" with each other properly, but scientists weren't sure
exactly how or why.

The malformed protein could actually be causing nerve cells to break
altogether, show the experiments announced today by scientists at the
University of Utah.

If Lincoln had the disease, it would explain the gangly walk for which
he was famous, they said.

Humans produce four protein genes called beta spectrin, which help our
cells regulate walking and talking and anything else requiring movement.
Normally, wire-like axons that connect each nerve cell flex and bend
when we do.

The mutation of one of the beta spectrin genes causes the degenerative
nerve disorder spinocerebellar ataxia type 5, which researchers at the
University of Minnesota found in 90 out of 299 of Lincoln's living
descendants in a 2006 test. Those afflicted with ataxia lose
coordination and sometimes end up confined to a wheelchair.

Until now, most scientists thought ataxia occurred because nerve cells
didn't have beta spectrin linking them together with the same strength
they do in a healthy individual.

Nematode worms also produce beta spectrin. When researchers removed the
beta spectrin gene from worms, however, the worms' wiry cell axons
didn't just malfunction — they severed.

The very same thing could be happening in humans, the University of Utah
biologists speculate.

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

The whisper-thin axon is the least complex part of a nerve cell,
Bastiani explained, so scientists often have looked elsewhere when
searching for the cause of nervous disorders such as ataxia.

Lincoln's trademark lumbering and awkward gait—noted by several
historians of his time—would have been a symptom of ataxia, said the
University of Minnesota researchers, whose hereditary study pegged his
chances of having the disease at about one-in-four.

If he did suffer from ataxia, it was probably in its early stages by the
time he was assassinated at age 56 in 1865, said Erik Jorgensen,
scientific director of the Brain Institute.

Most nerve cells in the worms studied weren't broken in the embryonic
stage, despite the lack of beta spectrin, but began snapping as the
worms grew larger. Beta spectrin is only necessary to prevent breakage
in mature cells and not to create new ones, the study showed.

Since it is continuous movement over time that causes axons to shatter,
without the protective coating of the protein Lincoln's unsteady and
irregular way of getting around would probably have gotten much worse
had he lived into old age.

The wayward beta spectrin gene could be the culprit in many other
neurodegenerative disorders, like Alzheimer's, the researchers said,
though further testing is needed.

The study's full findings are published in the most recent edition of
The Journal of Cell Biology.

© 2007 LiveScience.com

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shove a wooden cross up their arses and rotate
at a high rate of speed. I trust you'll
be 'blessed' with a plethora of splinters.