A gene produces a protein that keeps nerve cells flexible. When the gene was disabled in worms, their nerve cells broke. That may provide a new explanation for a disease identified in 11 generations of U.S. President Abraham Lincoln’s family.
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 new study will be published in The Journal of Cell Biology on Jan. 29, two weeks before Lincoln?s birthday on Feb. 12.
Bastiani calls it amazing that disease-causing nerve-cell damage may come in the form of broken axons ? the simplest part of a nerve cell. ?Everybody focuses on the synapse or the cell body as to where the action is,? he says. ?But if you break the wire or axon, the neuron doesn?t work anymore. It?s sort of the weakest link in the process.?