Nerve cells possess a protein that keeps nerve fibers flexible and a gene is responsible for the synthesis of this special type of protein, according to a study//.
A University of Utah study found that when the gene was disabled in tiny nematode worms, their nerve cells literally broke.
The discovery may provide a new explanation for spinocerebellar ataxia type 5 (SCA5), a disease previously tied to a human version of the gene and identified in 11 generations of U.S. President Abraham Lincoln's family, starting with his paternal grandparents. SCA5 may have afflicted Lincoln himself. The new study suggests how.
"Were Lincoln's nerves shattered? We don't know. But our study raises the possibility that they were," says biology Professor Michael Bastiani, the study's senior author and a member of the Brain Institute at the University of Utah.
The study involved a worm gene named unc-70 that makes a protein named beta spectrin. Humans have four beta spectrin genes, and mutations in one of them was identified previously as the cause of SCA5, a neurodegenerative disease that develops between ages 10 and 68; destroys nerve cells in the part of the brain that controls movements; causes loss of coordination in walking, speaking, writing and swallowing; and puts some patients in wheelchairs.
Earlier research showed beta spectrin makes red blood cells flexible so they don't burst, and that people with a beta spectrin mutation suffer a form of anemia.
The Utah biologists showed in nematode worms, frequently used as genetic stand-ins for humans, that loss of beta spectrin leaves neurons (nerve cells) prone to breakage. They found the microscopic protein acts like a tiny Slinky spring toy within the coating of nerve cells, giving them strength.
When 1-millimeter-long nematode worms were bred with the mutant gene, they lacked beta spectrin, resulting in breakage of their nerve cells' axons, the lPage: 1 2 3 Related medicine news :1
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