Biological aging, as opposed to the chronological kind we celebrate or curse annually, is what makes us describe some people as “ageless” and others as “old beyond their years.” We are collections of cells, and what happens in the cell doesn’t stay in the cell. It generates large-scale effects on our overall appearance, health and longevity.
A new study in JAMA indicates that otherwise healthy adults carrying a cellular signature of biological aging may be more vulnerable to infection and, once infected, more likely to exhibit symptoms. The experimenters first drew blood from 152 Pittsburgh residents, none of them over 55 years old, and dosed them with nose drops containing a common cold virus. Monitoring these volunteers for five days, the researchers took note of who sniffled and sneezed and who didn’t, and saw a correlation between study subjects’ susceptibility to the virus and a measure of biological aging called telomere shortening.
Telomeres, which cap the ends of each chromosome in every cell of all living creatures from fungi right on up to humans, are kind of like those plastic caps ringing each end of a shoelace. They stabilize chromosomes, keeping them from unraveling. (They prevent other damage, too.)
But telomeres aren’t so stable themselves. Rounds of cell division, bouts of stress, and episodes of inflammation cause them to shrink. If a telomere reaches a point where a chromosome’s integrity is challenged, the result could be cancer or some other malfunction in the cell housing the challenged chromosome.
Evolution has engineered protective mechanisms into cells so that if their telomeres get too short they die or, at least, lose their ability to divide any more. But this evolutionary emergency brake has its downside: It contributes to the slow but steady deterioration that manifests visibly in our aging skin and, less visibly, in all the other bodily organs.
In this case, the researchers were specifically interested in those bloodborne cells that comprise the immune system. But it’s widely believed that the state of telomeres in blood cells (the cells examined in the study) reflects their state in other tissues as well.
Just a week ago, a study in PLOS ONE led by Stanford psychopharmacologist Natalie Rasgon, MD, PhD, compared the telomeres in blood cells taken from high-functioning, well-educated, apparently fully healthy middle-aged women with a well-known genetic risk factor for late-onset Alzheimer’s disease (a good 15 percent of us are carriers) to those of otherwise matched non-carriers. The first group’s telomeres shortened by as much in two years as the second group’s did in ten, perhaps shedding some light on how this risk factor, called ApoE4, promotes cognitive decline. The good news was that the accelerated telomere shortening seen in ApoE4 carriers wasn’t observed if they’d been on estrogen-based hormone therapy at the onset of menopause and stayed on it for the study’s two-year duration.
While it might be nice to think longer telomeres are all it takes to ensure longevity, even the lengthiest telomeres are no match for a speeding truck. So be sure to look both ways before you cross the street.
Previously: Hormone therapy halts accelerated aging seen in women with Alzheimer’s genetic risk factor, Hormone therapy soon after menopause onset may reduce Alzheimer’s risk and Common genetic Alzheimer’s risk factor disrupts healthy older women’s brain function, but not men’s
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