University of Pittsburgh researchers have identified a region of one human chromosome — number 10 of the 23 we all carry — as the home of a gene associated with a high risk of Alzheimer’s disease.

People with both the newly identified gene and another genetic risk factor, called APOE E4, can have a 16-fold increase in their risk for the disease, the researchers say.

The finding could help single out individuals for participation in the growing number of studies of drugs to prevent or treat the mind-robbing condition, says study author Dr. George S. Zubenko, professor of psychiatry at the University of Pittsburgh, who describes the findings in the July issue of the journal Molecular Psychiatry.

Stories about chromosome 10 genes are not new. Last December, three groups of researchers reported similar discoveries about genes on the long arm of the X-shaped chromosome. But this report is different in several ways.

First, it looks at a different region — a relatively small stretch of DNA on the short arm of the chromosome. Second, it uses a method many scientists regard as quaintly out of date — following close relatives of Alzheimer’s patients for many years to see who develops the disease.

Finally, the work is so off the beaten path that it surprises D. Stephen Snyder, who as program director for the etiology of Alzheimer’s disease at the National Institute on Aging is in a position to know all about such research.

After a quick read of the paper and others that Zubenko has published, Snyder says, “It’s good science. The fruit is ripe for the picking, and I hope the study continues and gets stronger.”

He means that the 300 close relatives of Alzheimer’s patients Zubenko has followed for more than a decade are reaching the age when the condition becomes more common, so that the study could make an even stronger link between the pinpointed chromosome 10 region and risk of the disease.

That region, designated D10S1423, is “highly polymorphic,” meaning that its composition varies greatly from individual to individual, Zubenko says. He has established comparison standards for the people in the study, so that the work can be verified as individuals do or do not develop Alzheimer’s disease.

He says the next step is to “track our findings to a specific gene. That may give us opportunities for designing and evaluating treatments that delay the onset of Alzheimer’s disease.”

The designated region of the chromosome has five candidate genes, and Zubenko is using the new human genome map to single out the one linked to the increased risk.

He says the finding already “has potential in the design and testing of experimental treatments that are in the pipeline. It will help design trials with subjects with the greatest likelihood of responding to treatment.”

Snyder says that is important. “You don’t want to be giving someone a drug to which they will not respond because of their genetic makeup. If you narrow the field at the start, you have a better chance to get faster results,” he says.

Zubenko “should be lauded for his foresight in setting up the study. He is doing good things with a little out-of-date technology,” Snyder says.

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