Of the body’s some 25,000 genes, 28 in particular may be able to predict a person’s health span based solely on his or her molecular makeup, a new study finds.

Today’s research into aging doesn’t really care about life span anymore. Well, it does. Science wants you to live longer. But what it really cares about is the quality of your twilight years. For this, experts use the term “health span” — how old your body is on a molecular level, rather than how many birthdays you’ve celebrated. With the proper measurement tools, scientists speculate they’ll eventually be able to tell young patients, with certainty, their risks for neurological disease decades down the line.

"Imagine if we had biomarkers that tell doctors how you are doing in terms of aging, warning of any problems long before neurological deficits appear," said Northwestern University's Richard I. Morimoto, one of the senior authors of the new study, in a statement. The biomarkers Morimoto refers to are called molecular chaperones. As their name implies, they help protect the body’s cells from protein damage. Older humans have fewer chaperones, and those with degenerative diseases like Alzheimer’s have fewer still.

One of the key biomarkers for disease is the presence of misfolded proteins, which chaperones are in charge of preventing. "If this critical system declines," Morimoto said, "eventually tissues become dysfunctional and die. If we can keep the chaperones healthy, we should be able to keep the person healthy."

He and his colleagues wanted to home in on which chaperones played the biggest role in preserving a person’s health span. Through their genomic analyses and tests on human brain tissue, both healthy and diseased, the team landed on 28 chaperones that seemed to play the largest role in mitigating the risk of Alzheimer’s, Parkinson’s, and Huntington’s disease. They also used roundworm models, which have similar biochemical properties to human aging.

Working backward, the findings suggest a scientist could take a person’s blood sample and analyze it for specific chaperone biomarkers. If the levels indicated a health span outside the normal range, that scientist would know the person faced a greater risk for disease later in life. "Let's say a person is age 50, but we see his molecular chaperones have declined and aren't repairing proteins and cellular damage," Morimoto said. "The chaperones are acting more like age 85 or 90. That's a sign that medical intervention could help."

This bodes well for neurodegenerative disease research because the field is in dire need of preventive care. Many diseases don’t even carry any treatment options, let alone offer a cure. Patients are forced to enter palliative care and surrender to the inevitable slide into dementia, and eventually death. The best advice science can offer is to tell people to exercise often and investigate whether the disease runs in their family.

In the meantime, Morimoto and other like-minded scientists will continue researching how to exploit chaperones’ power as biomarkers for disease, though no one is tossing around the I-word — immortality — just yet. "The goal is not to make people live forever," he said, "but rather to match health span more closely with life span — to improve the quality of life being lived."

Source: Brehme M, Voisine C, Rolland T, et al. A Chaperome Subnetwork Safeguards Proteostasis in Aging and Neurodegenerative Disease. Cell Reports. 2014.