Aging is a highly complex process with thousands of genes influencing our health, which poses a challenge for researchers looking to explain and target the underlying processes that lead to declining health. Researchers from the Babraham Institute’s Epigenetics research program have published a map of genetic interactions in C. elegans in iScience which can be used to identify new genes that influence lifespan and that have equivalent genes in humans.

Researchers use simple model organisms like the nematode worm C. elegans to gather information that can inform studies on human aging because many genes are shared or have counterparts in other species. However, there are some conceptual and technical challenges that apply to the study of aging in model organisms. Dr. Casanueva, Group leader in the Epigenetics research program explains: “The way researchers usually study gene function is by disrupting its function and observing what happens. The disruption of some genes causes worms to live a very long-life. In this way, researchers have found the so-called ‘longevity-pathways.” However, the complexity underlying aging means that it is not enough to focus on individual genes. We need to study the overall organization of longevity by generating a systems-wide view.”

In collaboration with the physicist Marta Sales Pardo at University of Rovira i Virgili, Dr. Casanueva and her lab set out to cast a wider net when it comes to studying longevity genes. Together they created the largest network of gene regulatory interactions that are found in a long-lived type of C. elegans. In this network, the relationships between genes are represented by lines, and represented in different layers based on the flow of information between genes. The middle of the web represents the genes with the most influence, in this case, they receive complex input signals and de-code them, and connect to an output layer of genes. The researchers found that most key genes for longevity belong to transcription factors and metabolic genes.

Monash University, Australia scientists have discovered an enzyme that is key to why exercise improves our health. Importantly this discovery has opened up the possibility of drugs to promote this enzyme’s activity, protecting against the consequences of aging on metabolic health, including type 2 diabetes.

The proportion of people worldwide over 60 years old will double in the next three decades and by 2031, more than six million Australians will be over 65 years old. The incidence of type 2 diabetes increases with age so this aging population will also result in an increased incidence of the disease globally.

One of the main reasons for the increased prevalence of type 2 diabetes with age is the development of insulin resistance, or an inability for the body to respond to insulin, and this is often caused by reduced physical activity as we age.

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A team of researchers affiliated with a large number of institutions in Japan has developed a vaccine that tricks the immune system into removing senescent cells. In their paper published in the journal Nature Aging, the group describes their vaccine, how it works and how effective it was when given to test mice.

Prior research has shown that part of the aging process is the development of senescent cells —cells that outlive their usefulness but fail to die naturally. Instead, they produce chemicals that can lead to inflammation, aging and a host of other ailments. Prior research has shown that senescence occurs when cells stop dividing. Prior research has also shown that senescent cells can lead to tumor growth in some instances and tumor suppression in others. Senescence also plays a role in tissue repair, and its impacts on the body vary depending on factors such as overall health and age. It is suspected that senescence is related to telomere erosion, and in some cases, environmental factors that lead to cell damage. In this new effort, the researchers have developed a vaccine that creates antibodies that attach to senescent cells, marking them for removal by white blood cells.

The team was able to create the vaccine after identifying a protein made in senescent cells but not in healthy active cells. That allowed them to develop a type of vaccine based on the amino acids in the protein. When injected, the vaccine incites the body to produce antibodies that bind only to senescent cells, and that sets off an immune response that involves sending white blood cells to destroy the senescent cells.

Physical exercise is great for a mouse’s brain, and for yours. Numerous studies conducted in mice, humans and laboratory glassware have made this clear. Now, a new study shows it’s possible to transfer the brain benefits enjoyed by marathon-running mice to their couch-potato peers.

Stanford School of Medicine researchers have shown that blood from young adult mice that are getting lots of exercise benefits the brains of same-aged, sedentary mice. A single protein in the blood of exercising mice seems largely responsible for that benefit.

The discovery could open the door to treatments that—by taming brain inflammation in people who don’t get much exercise—lower their risk of neurodegenerative disease or slow its progression.

A team of researchers affiliated with a host of institutions in China and the U.S. has found that injecting procyanidin C1 (PCC1), a chemical found in grape seed extract, into older mice extended their lifespan. In their paper published in the journal Nature Metabolism, the group describes the link between PCC1 and extended lifespan in mice and the experiments they carried out with the material.

Scientists have been trying for many years to understand the aging process. The hope is that once it is understood, mitigation efforts can slow or stop the process to allow people to live longer or to live in a more healthy way as they age. In this new effort, the researchers screened 46 plant extracts looking for anti-aging capabilities. They came across PCC1. Initial tests during screening showed it reduced the number of senescent cells in the human prostate. Such cells are known to contribute to aging. Intrigued with their results, the researchers tested it further. They found that at low doses it prevented senescent cells from contributing to inflammation, and at higher doses killed them outright without harming other cells.

The team then injected 171 mice with PCC1, 91 of whom were considered to be old. They found that this increased the overall lifespan of the mice by 9 percent and their remaining lifespans by 60 percent, on average. The researchers also injected younger mice with the extract chemical over a period of four months and found it improved their physical fitness. They then injected mice that had cancerous tumors with the chemical and found that doing so helped to shrink tumors when given in conjunction with chemotherapy. They also found it did the same with human tumor cells implanted into mice.

As we age, our muscles gradually become smaller, weaker and less able to heal after injury. In a new study, UPMC and University of Pittsburgh researchers pinpoint an important mediator of youthfulness in mouse muscle, a discovery that could advance muscle regeneration therapies for older people.

Published today in Nature Aging, the study demonstrates that circulating shuttles called extracellular vesicles, or EVs, deliver genetic instructions for the longevity protein known as Klotho to muscle cells. Loss of muscle function and impaired muscle repair in old mice may be driven by aged EVs, which carry fewer copies of these instructions than those in young animals.

The findings are an important advance in understanding why the capacity for muscles to regenerate dwindles with age.

Cancer biologist Yibin Kang has disabled a key cancer gene MTDH in mice and in human tissue. A human treatment will be ready for human trials in a few years.

This could be the key to preventing or stopping cancer metastasis which is the primary cause of death due to cancer.

99% of breast cancer patients survive five years after diagnosis, only 29% do if the cancer has metastasized, according to current numbers from the National Cancer Institute.

Eliminating old, dysfunctional cells in human fat also alleviates signs of diabetes, researchers from UConn Health report. The discovery could lead to new treatments for Type 2 diabetes and other metabolic diseases.

The cells in your body are constantly renewing themselves, with older cells aging and dying as new ones are being born. But sometimes that process goes awry. Occasionally damaged cells linger. Called senescent cells, they hang around, acting as a bad influence on other cells nearby. Their bad influence changes how the neighboring cells handle sugars or proteins and so causes metabolic problems.

Type 2 diabetes is the most common metabolic disease in the US. About 34 million people, or one out of every 10 inhabitants of the US, suffers from it, according to the Centers for Disease Control and Prevention (CDC). Most people with diabetes have insulin resistance, which is associated with obesity, lack of exercise and poor diet. But it also has a lot to do with senescent cells in people’s body fat, according to new findings by UConn Health School of Medicine’s Ming Xu and colleagues. And clearing away those senescent cells seems to stop diabetic behavior in obese mice, they report in the 22 November issue of Cell Metabolism. Ming Xu, assistant professor in the UConn Center on Aging and the department of Genetics and Genome Sciences at UConn Health, led the research, along with UConn Health researchers Lichao Wang and Binsheng Wang as major contributors. Alleviating the negative effects of fat on metabolism was a dramatic result, the researchers said.

In a study published in Nucleic Acids Research, the team of cancer researcher Francis Rodier, an Université de Montréal professor, shows for the first time that cellular senescence, which occurs when aging cells stop dividing, is caused by irreversible damage to the genome rather than simply by telomere erosion.

This discovery goes against the scientific model most widely adopted in the last 15 years, which is based on one principle: telomeres, caps located at the ends of chromosomes whose purpose is to protect genetic information, erode with each cell division. When they get too short, they tell the cell to stop dividing, thus preventing damage to its DNA. Made dormant, the cell enters senescence.

For this model to be valid, the inactivation of a single telomere should be sufficient to activate the senescence program. Rodier’s laboratory and many others had already observed that several dysfunctional telomeres were necessary.

Many people develop Alzheimer’s or other forms of dementia as they get older. However, others remain sharp well into old age, even if their brains show underlying signs of neurodegeneration.

Among these cognitively resilient people, researchers have identified education level and amount of time spent on intellectually stimulating activities as factors that help prevent dementia. A new study by MIT researchers shows that this kind of enrichment appears to activate a gene family called MEF2, which controls a genetic program in the brain that promotes resistance to cognitive decline.

The researchers observed this link between MEF2 and cognitive resilience in both humans and mice. The findings suggest that enhancing the activity of MEF2 or its targets might protect against age-related dementia.