FINDINGS

Tuesday, January 30, 2007

Mad Cow Study Points To Virus, Not Proteins

Researchers have found more evidence that a virus may cause mad cow disease and a related brain disorder in humans, threatening to overturn 25 years of research focusing on malformed proteins called prions.

Nerve cells infected with the human form of mad cow disease contained a virus-size particle that doesn't appear in uninfected cells, said Laura Manuelidis, a neuropathologist at Yale Medical School. Cells infected with scrapie, a related sheep disorder, contained the same germ.

The findings challenge the idea that the diseases are spread by prions, abnormal proteins that have also been detected in the brains of infected humans and animals. Stanley Prusiner won the Nobel Prize in 1997 for research identifying prions as the infectious agent.

But questions have arisen because people and animals are thought to catch the disease by eating infected meat, and some researchers argue that the stomach and intestines would quickly break down any protein before it reached the blood or brain.

Delivery May Be Key In Infant Brain Bleeds

A study has found that about a quarter of babies born in vaginal deliveries had a small amount of bleeding in their brains while none delivered by Caesarean section did, but the researchers said it would be premature to view their findings as an endorsement of C-sections.

They said the findings, published in the journal Radiology, suggest brain bleeding in some newborns has been common in vaginal deliveries but is being detected now only because of sophisticated imaging technology.

"There's no evidence that these bleeds are associated with problems in later life in either mental or physical function or ability," said Honor Wolfe, an obstetrician at the University of North Carolina School of Medicine who worked on the study.

Ills of Lincoln Kin Tied To Broken Nerve Cells

A nervous-system disease that has affected 11 generations of Abraham Lincoln's family may be linked to a genetic mutation that causes nerve cells to break.

When the same gene was disabled in nematode worms, their nerve cells literally broke, and a University of Utah study said that finding could explain the origin of the disease called spinocerebellar ataxia Type 5.

"Were Lincoln's nerves shattered? We don't know, but our study raises the possibility that they were," said biology professor Michael Bastiani, lead author of the study, published yesterday in the Journal of Cell Biology.

-- From News Services


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