Blood proteins could be potential targets for future drugs to slow aging

Scientists have shown that two blood proteins have an impact on how long and healthy we live, according to research.

Developing drugs that target these proteins could be a way to slow the aging process, according to the largest genetic aging study.

As we age, after reaching adulthood, our bodies begin to deteriorate, leading to age-related diseases and death. This latest research examines which proteins might influence the aging process.

Many complex and related factors determine the rate at which we age and die, and these include genetics, lifestyle, environment, and chance. The study sheds light on the role proteins play in this process.

Some people naturally have higher or lower levels of certain proteins because of the DNA they inherited from their parents. These protein levels, in turn, can affect a person’s health.

Researchers at the University of Edinburgh have combined the results of six major genetic studies on human aging – each containing genetic information from hundreds of thousands of people.

Among 857 proteins studied, the researchers identified two that had significant negative effects on various measures of aging.

People who inherited DNA that causes elevated levels of these proteins were more frail, had poorer self-reported health, and were less likely to live exceptionally long lives than those who didn’t. .

The first protein, called apolipoprotein(a) (LPA), is made in the liver and is believed to play a role in blood clotting. High levels of LPA can increase the risk of atherosclerosis — a condition in which arteries become clogged with fatty substances. Heart disease and stroke are possible consequences.

The second protein, vascular cell adhesion molecule 1 (VCAM1), is found primarily on the surface of endothelial cells — a unicellular layer that lines blood vessels. The protein controls vasodilatation and contraction – and its role in blood clotting and the immune response.

VCAM1 levels rise when the body sends out signals that indicate it has detected an infection. VCAM1 then allows immune cells to cross the endothelial layer, as occurs in people with naturally low levels of these proteins.

The researchers say drugs used to treat disease by lowering levels of LPA and VCAM1 could have the added benefit of improving quality of life and length of life.

One such example is a clinical trial testing a drug that lowers LPA to reduce the risk of heart disease.

There are currently no clinical trials of VCAM1, but studies in mice have shown how antibodies that lower levels of this protein improve cognition as we age.

The results were published in the journal aging in nature.

Identifying these two key proteins could help extend healthy years of life. Drugs that lower these protein levels in our blood could allow the average person to live as healthy and as long as people who won the genetic lottery and were born with genetically low levels of LPA and VCAM1.”

dr Paul Timmers, Principal Investigator, MRC Human Genetics Unit, University of Edinburgh

Professor Jim Wilson, Chair of Human Genetics at the Usher Institute, University of Edinburgh, said: “This study demonstrates the power of modern genetics to identify two potential targets for future lifespan extension drugs.”


Magazine reference:

Timmer, PRHJ, et al. (2022) Mendelian randomization of genetically independent aging phenotypes identifies LPA and VCAM1 as biological targets for human aging. aging in nature.

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