Parasite Affords Extreme Lifespan to Ants

Parasite Affords Extreme Lifespan to Ants

When contemplating organisms with extreme lifespans, a variety of examples come to mind: naked mole rats (30 years), bowhead whales (200 years), and even humans (80 years) are exceedingly long-lived relative to animals similar in both size and genealogy. Ants are not often associated with extreme lifespan; the typical lifespan of a worker ant is 1-2 years. A queen ant, however, can live up to 30 times longer, an astounding fact when you consider that worker and queen ants are genetically identical. Recently, researchers have uncovered another phenomenon in the ant world whereby genetically identical individuals exhibit vastly different rates of aging. In a paper published in Royal Society Open Science, Beros et al. detail an example of the extreme lifespan extension imparted to normally short-lived worker ants that have been infected by the tapeworm Anomotaenia brevis.

AntIn the natural world, parasitism occurs quite frequently with a variety of outcomes, often negatively affecting the quality of life. In contrast, parasitism by A. brevis in worker ants of Temnothorax nylanderi results in a lifespan at least 3 times longer than that of uninfected workers, and potentially extending to equal that of a queen. While most parasites do not cause acute or catastrophic detriment to their host, often there is an observable impairment to either lifespan or fitness. Beros et al. note that occasionally there are instances in such host-parasite systems whereby lifespan extension is imparted to the host; however, these benefits come at the cost of reduced reproductive health. Curiously, their recent studies not only characterize a parasitic relationship that provides the benefit of a robust lifespan, but one in which there seems to be no trade-off in reproductive fitness. These parasitized workers actually seem to have increased reproductive potential when compared to other fertile, yet not actively breeding, members of the colony known as nurses.

In an attempt to determine a mechanism for this phenomenon, researchers measured a variety of metabolic, physiological, and social characteristics exhibited by infected and uninfected ants. According to their observations, physiological changes to infected workers result in a phenotype more characteristic of colony members belonging to the nurse caste, including similar metabolic rates, body mass, and lipid content. Additionally, infected workers have a changed cuticular hydrocarbon profile (chemical secretions similar to pheromones) seemingly resulting in greater social caretaking being afforded to them, which again is similar to their nurse-caste colony-mates.

Although infected workers appear most similar to nurses, there may be other factors at play as nurses do not exhibit lifespans similar to queens. Previous studies by the authors have observed changes in gene expression brought about by this particular host-parasite system. These changes could represent potential novel targets of future studies and lead to insights into areas of the aging process that are as yet unexplored.

Unraveling the mechanism by which a parasite extremely alters ant lifespans could be informative to potentially extending the human lifespan.

Can exercise prevent “inflamm-aging”?

Can exercise prevent “inflamm-aging”?

Researchers from Mayo Clinic have uncovered a novel way in which exercise may contribute to healthy aging by suppressing an age-related phenomenon known as the senescence-associated secretory phenotype, or SASP.

In recent years, research has uncovered a number of factors that contribute to or are present in the pathology of aging; among them, the SASP has gained a good deal of attention as a causal and potentially treatable contributor to the diseases of aging. Cellular senescence was first observed by Leonard Hayflick in 1965 and is characterized as a condition wherein a viable cell is no longer able to divide. As a result, cellular senescence is thought to act as a potential anti-cancer mechanism. Further, cellular senescence can result from a number of aberrant processes, including oxidative damage, mitochondrial dysfunction, telomere dysfunction, DNA damage/mutation, transcriptional dysregulation, and epigenetic dysregulation. Senescent cells have been observed to secrete a number of inflammatory hormones, and have therefore been implicated in driving what has been described as “inflamm-aging”, whereby chronic and unchecked inflammation leads to disease. These insights have led to a number of potentially promising interventions designed to remove or suppress senescent cells, referred to as senolytic or senomorphic therapies, respectively.

Exercise has long been attributed to improvements in health and longevity, and it has been hypothesized that these beneficial outcomes are due to improvements in a multitude of factors, including adiposity, cardiovascular health, and mitochondrial function. In their recent Aging Cell paper, Englund et al., have provided evidence for an additional mechanism by which exercise, via suppression of the SASP, may lead to benefits in aging populations. In this study, individuals undertook a 12-week progressive strength and endurance training program. As expected, study participants saw improvements in both physical performance and body composition measurements post-intervention when compared to their pre-intervention values. Additionally, levels of circulating CD3+ T-cells (cells involved in the adaptive immune response, targeting foreign agents) derived from peripheral blood showed decreased expression of SASP-associated mRNAs. Moreover, plasma-derived proteins known to be elevated as part of the SASP showed a significant reduction post-intervention.

While the authors note that previous interventional studies suggest that exercise may influence senescent cell burden, this had yet to be assessed in older adults utilizing known biomarkers. While the scope of this study does not address the mechanism (senolytic or senomorphic) by which exercise leads to a reduction in the SASP, the researchers demonstrate that exercise is effective in reducing SASP-associated biomarkers in older adults. Usefully, these biomarkers could aid researchers in determining the efficacy of future therapeutic interventions.

OFAS Hosting Session at AGE 47th Annual Meeting

OFAS Hosting Session at AGE 47th Annual Meeting

For years, Orentreich Foundation for the Advancement of Science has researched biomedical interventions to prevent, halt, or reverse those disorders that decrease the quality or length of life. Our groundbreaking research on dietary methionine restriction has shown its dramatic ability to increase longevity while improving healthspan, lowering body weight, and reducing the incidence of age-related diseases.

In addition to our dedication to discovery, we are also committed to promoting the exchange of knowledge and strengthening of relationships within the scientific community. We host a biennial symposium on healthy aging, support meetings in the field, and, each year, our scientists represent us at conferences and seminars around the globe.

This year, OFAS will host a pre-meeting session at the AGE 47th Annual Meeting in Philadelphia. The theme of the conference is “Improving Resiliency to Delay Aging”, and the OFAS-sponsored session is focused on Nutrition and Longevity. The panel of speakers includes: Dr. Sebastian Brandhorst from University of Southern California; Dr. John Newman from the Buck Institute and UCSF; Dr. John P. Richie from Penn State University; and Dr. Brian Kennedy from the Yong Loo Lin School of Medicine at the National University of Singapore.

How Mindfulness Protects You as You Get Older

How Mindfulness Protects You as You Get Older

In our minds, old age is often associated with negative outcomes, such as a decline in physical health, but research consistently finds that older adults tend to experience more positive emotion than their younger counterparts. In this study, older adults reported greater awareness of being in the present moment, also known as mindfulness, than younger adults. Furthermore, this mindfulness helped to explain why older adults reported more positive emotion than younger adults do, suggesting that mindfulness facilitates healthy aging.

The researchers asked participants about their mood, mindfulness, and perspective on the future to see how these factors might be related. The participants reported their current positive and negative emotions, such as enthusiasm, fear, interest, and hostility. They reflected on how much they were mindfully aware in the moment, rather than living in the past or anticipating the future. And participants considered whether they felt concerned about the limited time left in their life or positive about the opportunities awaiting them.

The older adults tended to recognize that they had fewer remaining years on earth than the younger participants, but they also felt greater positive emotion. And according to the researchers’ analysis, it was their focus on the here and now—their greater mindfulness compared to young people—that explained their good moods. The higher their mindfulness, the better they felt.  Since being mindful could help us regulate our emotions and relieve stress, it could be useful for humans to naturally grow in mindfulness as we get older. This is significant because positive emotions can also lead to better physical health. However, implications of these findings for health and well-being in younger and older adults are still being discussed.

Researchers Find Reversible Cause of Vascular Aging

Researchers Find Reversible Cause of Vascular Aging

The hallmarks of aging in skeletal muscle include endothelial cell dysfunction, impaired microcapillary formation, and a progressive decline in exercise capacity, yet the underlying causes of these symptoms are poorly understood. In a recent paper, researchers identify the mechanism behind vascular aging in mice and its effects on muscle health, and show the means by which they successfully reversed the process in animals.

The vascular aging process causes us to suffer from disorders such as cardiac and neurologic conditions, muscle loss, impaired wound healing, and overall frailty. As we age, our tiniest blood vessels wither and die, causing reduced blood flow and compromised oxygenation of organs and tissues. Endothelial cells are essential for the health and growth of the blood vessels that they line. Unfortunately, as these endothelial cells age, blood vessels deteriorate, new blood vessels fail to form, and blood flow to most parts of the body gradually diminishes. This process heavily affects the muscles, which are vascularized and rely on a robust blood supply to function. Exercise can slow the process, but over time, it becomes less effective.

The research team found that reduced blood flow develops as endothelial cells start to lose a critical protein known as SIRT1, which has been known to delay aging and extend life in yeast and mice. SIRT1 loss is precipitated by the loss of NAD+, a key regulator of protein interactions and DNA repair. Through a series of experiments, researchers found that NAD++ and SIRT1 provide a signaling network between endothelial cells in the walls of blood vessels and muscle cells, thus generating new capillaries to supply oxygen and nutrients to tissues and organs. By using an NAD++ precursor treatment in aging mice, the scientists saw a boost in the number of blood capillaries and capillary density, increasing the blood flow to muscles. These findings have implications for improving blood flow, increasing human performance, and reestablishing a cycle of mobility in the elderly, paving the way for therapies to address diseases that arise from vascular aging.