Vive Le Vin! UCLA Isolates Beneficial Wine Element

Researchers at UCLA say they have discovered the reason why people who drink red wine largely avoid heart disease, and may have come up with a naturally-occurring substance that can partly-reverse the effects of Alzheimer's disease.

UCLA neurology professor David Teplow said the discovery will now be tested in human subjects, and could be the first disease-modifying treatment of Alzheimer's. "We believe this is an important next step," he said.

The findings may explain why the typical diet in France, which is rich in bad cholesterol and saturated fats and copious amounts of red wine, does not lead to correspondingly-high levels of heart disease or Alzheimer's there.

Teplow and his team have measured how chemicals called polyphenols found in red wine block the formation of proteins that build up toxic plaque in the blood stream. This plaque has long been understood to clog arteries, and lead to Alzheimer's disease.

Writing in the latest Journal of Biological Chemistry, Teplow and his colleagues examined the 8,000 different types of polyphenols found in nature.

Foods such as cocoa, nuts, tea and berries contain polyphenols, and their link to plaque prevention has been long-understood.

The new research, conducted at UCLA and the Mt. Sinai School of Medicine in New York, is the first to explain the mechanics of how the various polyphenols work to combat plaque.

Using lab mice, the researchers monitored how two types of proteins found in human blood can cause heart disease or Alzheimer's. These proteins fold up and stick to each other in the blood, killing nerve endings and leading to heart disease or Alzheimer's.

Scientists used polyphenols distilled from grape seeds on the mice, and observed not only how the natural chemicals blocked the formation of the harmful proteins, but also reduced their toxicity, Peplow said.

In a statement released by UCLA, Teplow called the polyphenol's beneficial function "pretty straightforward" in blocking the proteins from converting into plaque-causing "toxic aggregates."

"If the proteins can't assemble, toxic aggregates can't form, and thus there is no toxicity," Teplow said. This "suggests that administration of the compound in Alzheimer's patients might block the development of these toxic aggregates, prevent disease development and also ameliorate existing disease."

Teplow's work was sponsored by grants from a wide-ranging group of federal agencies, the Japan Human Science Foundation, and the Alzheimer's Foundation. UCLA reported that Teplow has no financial ties with any agency that funded the research.