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Aging Research: Blood Proteins Show Your Age

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Blood Test for Aging
Credit: Adapted from iStock/jarun011

How can you tell how old someone is? Of course, you could scan their driver’s license or look for signs of facial wrinkles and gray hair. But, as researchers just found in a new study, you also could get pretty close to the answer by doing a blood test.

That may seem surprising. But in a recent study in Nature Medicine, an NIH-funded research team was able to gauge a person’s age quite reliably by analyzing a blood sample for levels of a few hundred proteins. The results offer important new insights into what happens as we age. For example, the team suggests that the biological aging process isn’t steady and appears to accelerate periodically—with the greatest bursts coming, on average, around ages 34, 60, and 78.

These findings indicate that it may be possible one day to devise a blood test to identify individuals who are aging faster biologically than others. Such folks might be at risk earlier in life for cardiovascular problems, Alzheimer’s disease, osteoarthritis, and other age-related health issues.

What’s more, this work raises hope for interventions that may slow down the “proteomic clock” and perhaps help to keep people biologically younger than their chronological age. Such a scenario might sound like pure fantasy, but this same group of researchers showed a few years ago that it’s indeed possible to rejuvenate an older mouse by infusing blood from a much younger mouse.

Those and other earlier findings from the lab of Tony Wyss-Coray, Stanford School of Medicine, Palo Alto, CA, raised the tantalizing possibility that certain substances in young blood can revitalize the aging brain and other parts of the body. In search of additional clues in the new study, the Wyss-Coray team tracked how the protein composition of blood changes as people age.

To find those clues, they isolated plasma from more than 4,200 healthy individuals between ages 18 and 95. The researchers then used data from more than half of the participants to assemble a “proteomic clock” of aging.  Within certain limits, the clock could accurately predict the chronological age of the study’s remaining 1,446 participants. The best predictions relied on just 373 of the clock’s almost 3,000 proteins.

As further validation, the clock also reliably predicted the correct chronological age of four groups of people not in the study. Interestingly, it was possible to make a decent age prediction based on just nine of the clock’s most informative proteins.

The findings show that telltale proteomic changes arise with age, and they likely have important and as-yet unknown health implications. After all, those proteins found circulating in the bloodstream come not just from blood cells but also from cells throughout the body. Intriguingly, the researchers report that people who appeared biologically younger than their actual chronological age based on their blood proteins also performed better on cognitive and physical tests.

Most of us view aging as a gradual, linear process. However, the protein evidence suggests that, biologically, aging follows a more complex pattern. Some proteins did gradually tick up or down over time in an almost linear fashion. But the levels of many other proteins rose or fell more markedly over time. For instance, one neural protein in the blood stayed constant until around age 60, when its levels spiked. Why that is so remains to be determined.

As noted, the researchers found evidence that the aging process includes a series of three bursts. Wyss-Coray said he found it especially interesting that the first burst happens in early mid-life, around age 34, well before common signs of aging and its associated health problems would manifest.

It’s also well known that men and women age differently, and this study adds to that evidence. About two-thirds of the proteins that changed with age also differed between the sexes. However, because the effect of aging on the most important proteins of the clock is much stronger than the differences in gender, the proteomic clock still could accurately predict the ages in all people.

Overall, the findings show that protein substances in blood can serve as a useful measure of a person’s chronological and biological age and—together with Wyss-Coray’s earlier studies—that substances in blood may play an active role in the aging process. Wyss-Coray reports that his team continues to dig deeper into its data, hoping to learn more about the origins of particular proteins in the bloodstream, what they mean for our health, and how to potentially turn back the proteomic clock.

Reference:

[1] Undulating changes in human plasma proteome profiles across the lifespan. Lehallier B, Gate D, Schaum N, Nanasi T, Lee SE, Yousef H, Moran Losada P, Berdnik D, Keller A, Verghese J, Sathyan S, Franceschi C, Milman S, Barzilai N, Wyss-Coray T. Nat Med. 2019 Dec;25(12):1843-1850. 

Links:

What Do We Know About Healthy Aging? (National Institute on Aging/NIH)

Cognitive Health (NIA)

Wyss-Coray Lab (Stanford University, Palo Alto, CA)

NIH Support: National Institute on Aging


Happy New Year: Looking Back at 2016 Research Highlights

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Science Breakthroughs of the Year 2016Happy New Year! While everyone was busy getting ready for the holidays, the journal Science announced its annual compendium of scientific Breakthroughs of the Year. If you missed it, the winner for 2016 was the detection of gravitational waves—tiny ripples in the fabric of spacetime created by the collision of two black holes 1.3 billion years ago! It’s an incredible discovery, and one that Albert Einstein predicted a century ago.

Among the nine other advances that made the first cut for Breakthrough of the Year, several involved the biomedical sciences. As I’ve done in previous years (here and here), I’ll kick off this New Year by taking a quick look of some of the breakthroughs that directly involved NIH support:


Cool Videos: Better Computation, Better Hope for Movement Disorders

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Video for OpenSimAvatar. Pick your Sim. The entertainment world has done an amazing job developing software that generates animated characters with strikingly realistic movement. But scientists have taken this one step further to create models that can help kids with cerebral palsy walk better, delay the onset of osteoarthritis, and even answer a question in the minds of children of all ages: How exactly did T. rex run?

That’s what the researchers behind this video—an entrant in the NIH Common Fund’s recent video competition—have done. They’ve developed OpenSim: a free software tool that combines state-of-the-art musculoskeletal modeling and dynamic computer simulations to produce highly accurate representations of the underlying biomechanics of motion. OpenSim was designed at the NIH-supported center for physics-based Simulation of Biological Structures (Simbios) at Stanford University, Palo Alto, CA. And now, researchers around the world are using OpenSim to find more effective interventions for a variety of movement disorders.

Links:

NIH Common Fund Video Competition

OpenSim (Stanford University, Palo Alto, CA)

NIH Support: Common Fund; Eunice Kennedy Shriver National Institute of Child Health and Human Development; National Institute for General Medical Sciences 


LabTV: Curious about Post-Traumatic Osteoarthritis

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LabTV-Avery White

If you like sports and you like science, I think you’ll enjoy meeting Avery White, an undergraduate studying biomedical engineering at the University of Delaware in Newark. In this LabTV profile, we catch up with White as she conducts basic research that may help us better understand—and possibly prevent—the painful osteoarthritis that often pops up years after knee injuries from sports and other activities.

Many athletes, along with lots of regular folks, are familiar with the immediate and painful consequences of tearing the knee’s cartilage (meniscus) or anterior cruciate ligament (ACL). Most also know that such injuries can usually be repaired by surgery. Yet, many people aren’t aware of the longer-term health threat posed by ACL and meniscus tears: a substantially increased risk of developing osteoarthritis years down the road—in some individuals, even as early as age 30. While treatments are available for such post-traumatic osteoarthritis, including physical therapy, pain medications, and even knee-replacement surgery, more preventive options are needed to avoid these chronic joint problems.

White’s interest in this problem is personal. She’s a volleyball player herself, her sister tore her ACL, and her mother damaged her meniscus. After spending a summer working in a lab, this Wilmington, DE native has grown increasingly interested in the field of tissue engineering. She says it offers her an opportunity to use “micro” cell biology techniques to address a “macro” challenge: finding ways to encourage the body to generate healthy new cells that may prevent or reverse injury-induced osteoarthritis.

What’s up next for White? She says maybe a summer internship in a lab overseas, and, on the more distant horizon, graduate school with the goal of earning a Ph.D.

Links:

LabTV

University of Delaware Biomedical Engineering

Science Careers (National Institute of General Medical Sciences/NIH)

Careers Blog (Office of Intramural Training/NIH)

Scientific Careers at NIH


Reprogramming Genes to Keep Joints Healthy

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Caption: [Left] The knee joint of a normal mouse that endured an ACL-type injury. The injury triggered osteoarthritis and caused the cartilage on the femur (red) and tibia (green) to degrade, allowing the bones to sandwich together. [Right] This is the knee joint of a mouse that received gene therapy after the ACL injury. The cartilage is thick and healthy, and covers the bones completely, providing a cushion.

Credit: Brendan Lee and Zhechao Ruan, Department of Molecular and Human Genetics,
Baylor College of Medicine, Houston, TX

 

Our joints are pretty amazing marvels of engineering, but they don’t last forever. As we age, or if we suffer certain injuries, the smooth, slippery white cartilage covering the ends of our bones begins to fray and degrade. This causes osteoarthritis (OA), or ‘wear-and-tear’ arthritis. As the cartilage thins and disappears, the bones can even grow spurs that grate against each other, causing swelling and pain. It’s a major cause of disability, and there’s currently no cure—other than joint replacement, which is a pretty big deal and isn’t available for all joints. About 27 million Americans already have osteoarthritis; about 1 in 2 will suffer from some form of the disease over their lifetime. Those are lousy odds.