Lifeboat Foundation

Research conducted by Qiang et al has discovered a link between a protein in red blood cells and age-related decline in cognitive performance. Published in the open access journal PLOS Biology on 17th June 2021, the study shows that depleting mouse blood of the protein ADORA2B leads to faster declines in memory, delays in auditory processing, and increased inflammation in the brain.

As life expectancies around the world increase, so are the number of people who will experience age-related cognitive decline. Because the amount of oxygen in the blood also declines with age, the team hypothesized that aging in the brain might be naturally held at bay by adenosine receptor A2B (ADORA2B), a protein on the membrane of red blood cells which is known to help release oxygen from the blood cells so it can be used by the body. To test this idea, they created mice that lacked ADORA2B in their blood and compared behavioral and physiological measures with control mice.

The team found that as the mice got older, the hallmarks of cognitive decline—poor memory, hearing deficits, and inflammatory responses in the brain—were all greater in the mice lacking ADORA2B than in the control mice. Additionally, after experiencing a period of oxygen deprivation, the behavioral and physiological effects on young mice without ADORA2B were much greater than those on normal young mice.

BES/BZR転写因子ファミリー間の競合関係は維管束幹細胞の増殖と分化のバランスを安定化させ幹細胞の永続的な維持に貢献する。

A new study led by University of Maryland and UCLA researchers found that DNA from tissue samples can be used to accurately predict the age of bats in the wild. The study also showed age-related changes to the DNA of long-lived species are different from those in short-lived species, especially in regions of the genome near genes associated with cancer and immunity. This work provides new insight into causes of age-related declines.

This is the first research paper to show that animals in the wild can be accurately aged using an epigenetic clock, which predicts age based on specific changes to DNA. This work provides a new tool for biologists studying animals in the wild. In addition, the results provide insight into possible mechanisms behind the exceptional longevity of many bat species. The study appears in the March 12, 2021, issue of the journal Nature Communications.

“We hoped that these epigenetic changes would be predictive of age,” said Gerald Wilkinson, a professor of biology at UMD and co-lead author of the paper. “But now we have the data to show that instead of having to follow animals over their lifetime to be sure of their age, you can just go out and take a tiny sample of an individual in the wild and be able to know its age, which allows us to ask all kinds of questions we couldn’t before.”

The inside of a mitochondria is made up of a folded membrane, which has evolved to produce the greatest surface area possible between two parts of the mitochondria known as the intermembrane space (the outer part) and the mitochondrial matrix (the inner part). To drastically oversimplify this entire process, the mitochondria uses glucose (and ethanol if it’s available) to pump hydrogen ions (with the occasional deuterium and tritium ion) across the membrane which separates these two compartments of the mitochondria (known as the cristae) into the intermembrane space. These hydrogen ions then flow back into the mitochondrial matrix through a very special protein called ATP synthase, which uses the electrostatic potential energy of the hydrogen ion to manufacture ATP.

Unfortunately, as we get older this inner membrane starts to decay and become smaller. As the cristae starts to shrink, there is less space for ATP synthase, which means there is less ATP produced, which ultimately means that our cells do not have enough energy to maintain all of our cellular functions. As you can imagine, this lack of energy is catastrophic for the health of the cell, and will eventually lead to either cell senescent (where the cell essentially becomes dormant), or complete cell death.

Numerous different suggestions have been put forward as to explain why exactly why mitochondria decay in this way, including mutations within the DNA of the mitochondria (they have their own chromosomes), as well as the build up of oxidative agents within the cell itself which cause direct damage to the mitochondria. However, a group of scientists lead by Dr Hazel Szeto have discovered that the decay of the mitochondrial cristae is linked to declining levels of a phospholipid (fat) called cardiolipin. It turns out that as we age, oxidative agents within our body destroy this phospholipid, which is essential for maintaining the folded inner membrane of the mitochondria.

Several different causes of aging have been discovered, but the question remains whether there are common underlying mechanisms that determine aging and lifespan. Researchers from the Max Planck Institute for Biology of Ageing and the CECAD Cluster of Excellence in Ageing research at the University Cologne have now come across folate metabolism in their search for such basic mechanisms. Its regulation underlies many known aging signaling pathways and leads to longevity. This may provide a new possibility to broadly improve human health during aging.

In recent decades, several cellular signaling pathways have been discovered that regulate the lifespan of an organism and are thus of enormous importance for aging research. When researchers altered these signaling pathways, this extended the lifespan of diverse organisms. However, the question arises whether these different signaling pathways converge on common metabolic pathways that are causal for longevity.

We probably cannot slow the rate at which we get older because of biological constraints, an unprecedented study of lifespan statistics in human and non-human primates has confirmed.

The study set out to test the ‘invariant rate of aging’ hypothesis, which says that a species has a relatively fixed rate of aging from adulthood. An international collaboration of scientists from 14 countries, including José Manuel Aburto from Oxford’s Leverhulme Centre for Demographic Science, analyzed age-specific birth and death data spanning centuries and continents. Led by Fernando Colchero, University of Southern Denmark and Susan Alberts, Duke University, North Carolina, the study was a huge endeavor requiring monitoring wild populations of primates over several decades.

Jose Manuel Aburto says, Our findings support the theory that, rather than slowing down death, more people are living much longer due to a reduction in mortality at younger ages. We compared birth and death data from humans and non-human primates and found this general pattern of mortality was the same in all of them. This suggests that biological, rather than environmental factors, ultimately control longevity.

With heart donors in short supply, artificial hearts have literally been a lifesaver for many heart patients. Here’s all you need to know about them.

Stem cell biologist Hugo Vankelecom (KU Leuven) and his colleagues have discovered that the pituitary gland in mice ages as the result of an age-related form of chronic inflammation. It may be possible to slow down this process or even partially repair it. The researchers have published their findings in PNAS.

The pituitary gland is a small, globular gland located underneath the brain that plays a major role in the hormonal system, explains Professor Hugo Vankelecom from the Department of Development and Regeneration at KU Leuven. “My research group discovered that the pituitary gland ages as a result of a form of chronic inflammation that affects tissue and even the organism as a whole. This natural process usually goes unnoticed and is referred to as ‘inflammaging’—a contraction of inflammation and aging. Inflammaging has previously been linked to the aging of other organs.” Due to the central role played by the pituitary, its aging may contribute to the reduction of hormonal processes and hormone levels in our body—as is the case with menopause, for instance.

The study also provides significant insight into the stem cells in the aging pituitary gland. In 2012, Vankelecom and his colleagues showed that a prompt reaction of these stem cells to injury in the gland leads to repair of the tissue, even in adult animals. “As a result of this new study, we now know that stem cells in the pituitary do not lose this regenerative capacity when the organism ages. In fact, the stem cells are only unable to do their job because, over time, the pituitary becomes an ‘inflammatory environment’ as a result of the chronic inflammation. But as soon as the stem cells are taken out of this environment, they show the same properties as stem cells from a young pituitary.”

In a minute and 27 seconds we get the what from an eye regeneration for mice, to monkey trials to start later this year, to human trials by 2023, and full body in a decade.

David Sinclair—a world-leading biologist, Harvard Medical School Professor, and author of The New York Times best-selling book @Lifespan.

Continue reading “When can we begin to apply age reversal gene therapies to humans? Harvards David Sinclair explains” »