news20090908sn

[SN Today] from [ScienceNews]

[SN Tosay]
Blue halos of doom
Under ultraviolet light, rings around the brown spots in aging bananas may signal the transition from ripe to rotten
By Jenny Lauren Lee
Web edition : Monday, September 7th, 2009

Ghostly rings of light surround the dying brown spots in overly ripe bananas, researchers report. The halos, which glow intensely blue under ultraviolet light, may mark the beginnings of cell death and may signal to animals such as apes that the bananas are ready for eating.

Bernhard Kräutler of the University of Innsbruck in Austria and his colleagues had already found that yellow bananas have a blue hue under UV light. Green bananas, on the other hand, don’t. The blue, the researchers knew, comes from a class of fluorescent chemicals that are produced and build up when chlorophyll breaks down.

In the new study, reported online September 7 in Proceedings of the National Academy of Sciences, the team determined what happens under UV light when the bananas become overripe. Though the brown spots themselves are dull, the team found that a ring of flesh surrounding the spots glows with an intensity three times that of the yellow peel. By analyzing the light, the researchers found that the chlorophyll-breakdown chemicals were more abundant in the rings than elsewhere in the banana.

Scientists do not yet know if the halo serves any biological purpose for the bananas. But Kraeutler speculates that animals may use the light to see whether fruit is ripe or rotten.

For example, he says, scientists have postulated that apes use color vision to detect fruit in the woods and that they see short-wavelength light, such as blue light verging on ultraviolet, better than humans do. “There’s a very high correlation between the ability to see fruit and the development of color vision,” Kraeutler says.

The halos may also provide a way for researchers to study cell death in bananas, and possibly other plants, without resorting to invasive procedures.

So far these fluorescing by-products of chlorophyll breakdown have only been found to accumulate in one other plant, the peace lily. The fluorescing chemicals, though briefly present, also do not seem to build up a glow in apples and pears.


[SN Today]
Three genes linked to Alzheimer’s disease risk
Genome studies highlight gene variants that may give new directions to studies of the neurodegenerative disorder
By Tina Hesman Saey
Web edition : Monday, September 7th, 2009

Scientists have a new lead on genes that contribute to the risk of developing Alzheimer’s disease.

Comparing subtle genetic spelling variations in nearly 12,000 Alzheimer’s patients with almost 19,000 other people revealed three genes associated with the disease, two international teams of researchers report online September 6 in Nature Genetics.

These genes are the first to be implicated in the risk of getting the common form of Alzheimer’s since the variant of the apolipoprotein E gene APOE4 was identified in 1993. That gene’s influence may explain about 20 percent of cases of Alzheimer’s disease, says Philippe Amouyel of the French health research agency INSERM in Lille and coauthor of one of the new studies. But researchers knew other genes must be involved since 60 to 80 percent of the risk of developing the disease is genetic.

“If there were another gene that had the large effect like APOE, we would have seen it already,” says John C. Morris, director of the Alzheimer’s research center at Washington University in St. Louis. Since no other genes stood out, scientists decided to take a statistical approach and look for common variants of genes that could have subtle influence on the development of the disease.

Both groups found single “letter” differences, called single nucleotide polymorphisms or SNPs, in the DNA surrounding the gene for clusterin. Also known as CLU or APOJ, clusterin is thought to help remove the plaque-forming molecule amyloid-beta from the brain. Amyloid-beta molecules clump together and somehow kill neurons in a process that isn’t fully understood (SN: 8/16/08, p. 20).

The two studies “are remarkably consistent with each other,” says Caleb Finch, a neuroscientist at the University of Southern California in Los Angeles who was not involved in either of the studies. Finch predicts that the new studies will kindle more interest in the neurobiology of clusterin, a protein that his previous work has suggested may be important. It’s still not clear exactly how the new variant affects levels of the protein in the brain, he says.

“I’m open-minded about further complexities in the clusterin story and about further gene candidates,” he says.

In one of the new studies, a group led by Julie Williams of Cardiff University in Wales also discovered variants near a gene encoding the PICALM protein, short for phosphatidylinositol-binding clathrin assembly protein. That protein is involved in “controlling what gets into the cells and how it is transported to the rest of the cell,” Williams says. PICALM may help regulate the entry of a precursor to amyloid-beta into neurons, and also participates in regulating communications between neurons.

Amouyel’s group identified a third gene variant linked to a reduced risk of Alzheimer’s disease. Called CR1, the complement component receptor gene codes for an immune system protein that punches holes in invading bacteria and plays a role in inflammation. Inflammation has been fingered as a probable culprit in the development of Alzheimer’s, but studies of inflammation have produced mixed results. On one hand, inflammation is necessary to clear amyloid-beta and other toxic debris from the brain. But too much inflammation damages tissues, Williams says. The form of CR1 identified in the study seems to have a protective effect against developing Alzheimer’s disease, but the researchers don’t yet know if the variant increases or decreases inflammation, she says.