A new study lends additional evidence to the likelihood that genes associated with high levels of the so-called good cholesterol appear to contribute to exceptionally long life expectancy and resistance to age-related disease.

Sofiya Milman , an assistant professor of medicine in geriatrics and endocrinology at Albert Einstein College of Medicine in New York, said her team’s findings could open the way to finding drugs that target the gene and mimic its functions, thereby extending life.

“These genotypes may explain the mechanisms responsible for the beneficial HDL,” Milman said, saying further study of the genes could help unlock the secrets of what she called “successful agers.” One of the gene variants related to HDL cholesterol appeared to not only contribute to longer life, but to protect older people from age-related cognitive impairment, she said.

But Milman also cautioned that studies with larger sample sizes and more diverse populations should be conducted to validate the results.

Milman’s research was one of several presentations on the science of aging offered Thursday at the annual meeting of the Gerontological Society of America’s annual scientific conference at the Walter E. Washington Convention Center. The conference, which opened Wednesday, draws about 4,000 researchers. More than 500 presentations of original research are scheduled before the conference ends Sunday.

The Einstein study focused on 300 women and 94 men who were at least 95 years old and living independently when the study began in 1998. All of the people were from the northeastern United States and all were Jews of European descent, a factor that was useful because of the relative homogeneity of their genetics.

Researchers then monitored the participants until the participants’ deaths, focused on their levels of HDL, which stands for high-density lipoprotein. HDL , helps the body regulate and maintain the level of cholesterol, an important component of health. Cholesterol, which is found in certain foods and created by the body itself, helps create hormones, synthesizes vitamin D, and builds and maintains cell membranes.

To transport and store cholesterol, the liver transforms it into lipoproteins. Low-density lipoproteins (LDL) carry cholesterol to the body’s cells; HDL moves through the bloodstream acting as a scavenger that returns cholesterol to the liver for excretion or recycling.

The Einstein team theorized that long life might be linked to high HDL levels and the presence of a gene variant of an enzyme – known as CETP, or cholesterol ester transfer protein – that transfers cholesterol between HDL particles and LDL particles circulating in the bloodstream.

The team also looked at a gene variant known as apolipoprotein 1 (APOA1), which codes for a protein that is a major component in HDL, to see whether that too might be a marker for exceptional longevity.

The team measured the participants’ HDL levels and put them into two groups defined by relatively high or relatively low HDL levels.

The researchers discovered that the average lifespan of those with the favorable CETP gene variant was eight months longer compared to those without it – a striking finding given that these people were among a group of others who had also pushed beyond the limits of normal life expectancy. Those with the favorable variant of the APOA1 gene also had a longer lifespan, though slightly less than with the CETP variant.