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A new, very good article on aging, modern aging research and its history, RAAD feest and other initiatives, on model organisms, genetics and future lifespans. “… In early December 2018, just a few months after RAADfest, I visited the Buck Institute for a daylong symposium titled “Live Better Longer: A Celebration of 30 Years of Research on Aging.” That wasn’t an arbitrary demarcation: Aging is one of the rare areas of modern science with a specific launch date. In this case, it was January 1988, when Tom Johnson, a behavioral geneticist at the University of California, Irvine, published a paper that linked a genetic mutation he named “age-1” to longer lifespans in a transparent, microscopic, mostly hermaphroditic roundworm known in scientific circles as C. elegans. Prior to Johnson’s discovery, aging had not received a lot of attention from researchers. In the 1820s, Benjamin Gompertz, a self-trained mathematician, concluded that humans don’t start to break down at some magic age but are constantly declining and losing the ability to repair themselves, a concept now referred to as the Gompertz law of mortality. The first hint that there might be a cellular mechanism underlying the aging process came more than a century later, in the 1930s, when two Cornell scientists discovered that rats kept on calorically restricted diets lived significantly longer than their more satiated brethren. But overall, the field was mostly known as being a haven for charlatans and quacks peddling immortality elixirs and other magical cures — a reputation that continued even after Johnson’s work was published…In 1993, Cynthia Kenyon, an assistant professor at the University of California, San Francisco, discovered that mutations on a different gene, called daf-2, caused C. elegans to live twice as long as expected. Several years later, Gary Ruvkun, a researcher at Harvard Medical School, showed that these so-called worm-aging genes were closely related to genes in the insulin-signaling system of humans. Around the same time, MIT’s Guarente and some of his colleagues discovered the first of several genes in yeast — which are also present in humans — linked to dramatically extended lifespan…” https://medium.com/s/2069/how-long-will-we-live-in-2069-f03e698f6de2


With this promising research on the horizon, how long might humans live in the future? Fantastical claims to longevity have existed since the dawn of recorded time, but reliable data about maximum human lifespan only dates to the mid-1950s, when the Guinness Book of World Records began independently verifying claims. Even then, initially corroborated ages can end up disproven: On December 27, Russian researchers published a paper arguing that the current world record holder, a Frenchwoman named Jeanne Calment, who said she was 122 when she died in 1997, had stolen her mother’s identity and was actually 99 at the time.

Assuming Calment wasn’t a fraud, since 1955, 46 people have made it to age 115. Nine of them have made it to 117 — and only two, Calment and an American woman named Sarah Knauss, have made it past 117. (Knauss died in 1999 at age 119). Over that same time frame, just under 11 billion people have been alive. That means roughly .0000004204133 percent of people have made it to 115. You’re 79,333 times more likely to get hit by lightning than you are to live to 115; 22,455 times more likely to end up in the emergency room from a golf cart accident; and 11,817 times more likely to get murdered.

That’s why 115 to 125 is often used as a range for the maximum human lifespan. Some researchers believe that supercentenarians, similar to naked mole rats, are impervious to major age-related diseases like cancer, Parkinson’s, and Alzheimer’s until just before they die. If scientists can figure out how to disrupt the underlying mechanisms that cause our cells to age, the thinking goes, then supercentenarians will become as common as 80-year-olds are today.

In a study published in Environment International researchers at Karolinska Institutet in Sweden show how PFAS industrial chemicals, which are used in many consumer products, pass through the placenta throughout pregnancy to accumulate in fetal tissue. Further research is now needed to ascertain the effect that highly persistent PFAS chemicals have on the fetus.

The PFAS () group comprises thousands of human-made chemicals, which, thanks to their water- and grease-resistant properties, are used in everything from frying pans and food packaging to clothes, cleaning agents and firefighting foams.

“We’ve focused on six of these PFAS substances and found that all appear to the same extent in as in the placenta,” says Richelle Duque Björvang, doctoral student at the Department of Clinical Science, Intervention and Technology, Karolinska Institutet. “So when the baby is born, it already has a build-up of these chemicals in the lungs, liver, brain, and elsewhere in the body.”

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(CNN) — Intensive lowering of blood pressure, to a less than 120 mm Hg level, can have a measurable impact on mild cognitive impairment (MCI) — a well-established precursor of dementia, a new study finds.

Previous studies have suggested high blood pressure could be a risk factor for dementia and mild cognitive impairment, leading US researchers to explore whether lowering pressure could reduce this risk in a large randomized trial on more than 9000 people.

Lowering blood pressure did not significantly reduce dementia risk, but the secondary results showed a significant reduction in MCI, according to the study published Monday.

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The gut microbiome is made up of billions of bacteria, and scientists have been trying to understand exactly how they affect our health, contribute to our risk of contacting diseases and how they interact with the vital organs and systems in the body, including the brain. It is quite a lot to unpick.


As countries industrialise, their air becomes dirtier – and this could have some far-reaching effects on the beneficial bacteria inside us.

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Monitoring their sleeping patterns, researchers identified an increase in the duration and continuity of REM sleep and specific brain oscillations characteristic of REM sleep, whereas ‘deep’ sleep, or non-REM sleep, did not change. The changes in REM sleep were very tightly linked to deficiency in the regulation of the stress hormone corticosterone. Mild stress also caused changes in gene expression in the brain.


The first and most distinct consequence of daily mild stress is an increase in rapid-eye-movement (REM) sleep, a new study in the journal PNAS reports. The research also demonstrated that this increase is associated with genes involved in cell death and survival.

REM sleep, also known as paradoxical sleep, is the sleep state during which we have most of our dreams and is involved in the regulation of emotions and memory consolidation. REM sleep disturbances are common in mood disorders, such as depression. However, little was known about how sleep changes are linked to molecular changes in the brain.

During this 9-week study, conducted by researchers from the Surrey Sleep Research Centre at the University of Surrey in collaboration with Eli Lilly, mice were intermittently exposed to a variety of mild stressors, such as the odour of a predator. Mice exposed to mild stressors developed signs of depression; they were less engaged in self-care activities; were less likely to participate in pleasurable activities such as eating appetising food, and became less social and interested in mice they hadn’t encountered before.

Decoder, developed in collaboration with a games developer, gets users to assume the role of an intelligence officer tasked with breaking up global criminal gangs (users are able to select a character and their backstory).

To meet the objective, users have to identify different combinations of number strings in missions littered with distraction.

Winning each mission means users unlock letters of the next criminal location (the higher the score, the more letters revealed).

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The adult brain has learned to calculate an image of its environment from sensory information. If the input signals change, however, even the adult brain is able to adapt − and, ideally, to return to its original activity patterns once the perturbation has ceased. Scientists at the Max Planck Institute of Neurobiology in Martinsried have now shown in mice that this ability is due to the properties of individual neurons. Their findings demonstrate that individual cells adjust strongly to changes in the environment but after the environment returns to its original state it is again the individual neurons which reassume their initial response properties. This could explain why despite substantial plasticity the perception in the adult brain is rather stable and why the brain does not have to continuously relearn everything.

Everything we know about our environment is based on calculations in our brain. Whereas a child’s brain first has to learn the rules that govern the environment, the adult brain knows what to expect and, for the most part, processes environmental stimuli in a stable manner. Yet even the adult brain is able to respond to changes, to form new memories and to learn. Research in recent years has shown that changes to the connections between neurons form the basis of this plasticity. But, how can the brain continually change its connections and learn new things without jeopardizing its stable representation of the environment? Neurobiologists in the Department of Tobias Bonhoeffer in Martinsried have now addressed this fundamental question and looked at the interplay between plasticity and stability.

The scientists studied the stability of the processing of sensations in the visual cortex of the mouse. It has been known for about 50 years that when one eye is temporarily closed, the region of the brain responsive to that eye increasingly becomes responsive to signals from the other eye that is still open. This insight has been important to optimize the use of eye patches in children with a squint. “Thanks to new genetically encoded indicators, it has recently become possible to observe reliably the activity of individual neurons over long periods of time,” says Tobias Rose, the lead author of the study. “With a few additional improvements, we were able to show for the first time what happens in the brain on the single-cell level when such environmental changes occur.”

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