The team’s critical insight was to construct a “viral language” of sorts, based purely on its genetic sequences. This language, if given sufficient examples, can then be analyzed using NLP techniques to predict how changes to its genome alter its interaction with our immune system. That is, using artificial language techniques, it may be possible to hunt down key areas in a viral genome that, when mutated, allow it to escape roaming antibodies.
It’s a seriously kooky idea. Yet when tested on some of our greatest viral foes, like influenza (the seasonal flu), HIV, and SARS-CoV-2, the algorithm was able to discern critical mutations that “transform” each virus just enough to escape the grasp of our immune surveillance system.
Summary: Better glucose uptake compensates for age-related motor deterioration and extends lifespan in fruitflies.
Source: Tokyo Metropolitan University.
Researchers from Tokyo Metropolitan University have discovered that fruit flies with genetic modifications to enhance glucose uptake have significantly longer lifespans.
No that’s not clickbait. Being able to stop and reverse aging is probably something every single person has yearned for at some point in their life. Now researchers are finally seeing successful implementations of methods for reversing aging in Animal cells. This creates the potential for countless benefits for humans. These range from simply preventing age related illness all the way to allowing women the opportunity to have kids at any point in their life when they are ready. We are living in very exciting scientific times.
References:
Reprogramming to recover youthful epigenetic information and restore vision — https://doi.org/10.1038/s41586-020-2975-4
NAD+ Repletion Rescues Female Fertility during Reproductive Aging — https://doi.org/10.1016/j.celrep.2020.01.
Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16 — https://doi.org/10.1007/s10522-009-9225-3
Researchers from Tokyo Metropolitan University have discovered that fruit flies with genetic modifications to enhance glucose uptake have significantly longer lifespans. Looking at the brain cells of aging flies, they found that better glucose uptake compensates for age-related deterioration in motor functions, and led to longer life. The effect was more pronounced when coupled with dietary restrictions. This suggests healthier eating plus improved glucose uptake in the brain might lead to enhanced lifespans.
The brain is a particularly power-hungry part of our bodies, consuming 20% of the oxygen we take in and 25% of the glucose. That’s why it’s so important that it can stay powered, using the glucose to produce adenosine triphosphate (ATP), the “energy courier” of the body. This chemical process, known as glycolysis, happens in both the intracellular fluid and a part of cells known as the mitochondria. But as we get older, our brain cells become less adept at making ATP, something that broadly correlates with less glucose availability. That might suggest that more food for more glucose might actually be a good thing. On the other hand, it is known that a healthier diet actually leads to longer life. Unraveling the mystery surrounding these two contradictory pieces of knowledge might lead to a better understanding of healthier, longer lifespans.
A team led by Associate Professor Kanae Ando studied this problem using Drosophila fruit flies. Firstly, they confirmed that brain cells in older flies tended to have lower levels of ATP, and lower uptake of glucose. They specifically tied this down to lower amounts of the enzymes needed for glycolysis. To counteract this effect, they genetically modified flies to produce more of a glucose-transporting protein called hGut3. Amazingly, this increase in glucose uptake was all that was required to significantly improve the amount of ATP in cells. More specifically, they found that more hGut3 led to less decrease in the production of the enzymes, counteracting the decline with age. Though this did not lead to an improvement in age-related damage to mitochondria, they also suffered less deterioration in locomotor functions.
Important here is at 38:13 where he says not only is his TAME trial paid for but an organization is going to pay a billion dollars per year on aging. He was not allowed to give details but it was going to start this month. I’ll be watching for the news.
Dr. Nir Barzilai discusses the TAME Trial and what this group may learn from the successes for advancing progress on biomarkers in particular and on aging in general.
About Nir Barzilai:
Nir Barzilai, MD, is a Professor in the Department of Endocrinology Medicine and the Department of Genetics at the Albert Einstein College of Medicine. He is also the Ingeborg and Ira Leon Rennert Chair of Aging Research at the Albert Einstein College of Medicine.
Dr. Barzilai is the founding director of the Institute for Aging Research at Albert Einstein College of Medicine and the Director of the Nathan Shock Center for Excellence in the Basic Biology of Aging, funded by the National Institutes of Health (NIH); the center is coordinating 80 investigators and six program projects on the biology of aging. He is also the director of the Glenn Center of Excellence in the Biology of Human Aging. He is a chaired professor of medicine and of genetics and a member of the Diabetes Research Center and the divisions of endocrinology and geriatrics.
Dr. Barzilai’s interests focus on several basic mechanisms in the biology of aging, including the biological effects of nutrients on extending life and the genetic determinants of life span. His team discovered many longevity gene in humans, and they further characterized the phenotype and genotype of humans with exceptional longevity through NIH awards. He also has an NIH Merit award investigating the metabolic decline that accompanies aging and its impact on longevity.
Dr. Barzilai has published more than 270 peer-reviewed papers, reviews and chapters in textbooks. Dr. Barzilai serves on several editorial boards and advisory boards of pharmaceutical and start-up companies, and is a reviewer for numerous journals. A Beeson Fellow for Aging Research, Dr. Barzilai has received many other prestigious awards, including the Senior Ellison Foundation Award, the 2010 Irving S. Wright Award of Distinction in Aging Research, the NIA–Nathan Shock Award and a merit award from the NIA for his contributions in elucidating metabolic and genetic mechanisms of aging and was the 2018 recipient of the IPSEN Longevity award. He is leading the TAME (Targeting/Taming Aging with Metformin) Trial, a multi-center study to prove the concept that multi morbidities of aging can be delayed in humans and change the FDA indications to allow for next generation interventions.
A team of researchers at Columbia University has developed a way to allow DNA strands to store more data. In their study, published in the journal Science, the group applied a small amount of electricity to DNA strands to allow for encoding more information than was possible with other methods.
For several years, researchers have been looking for ways to increase data storage capacity—storage requirements are expected to exceed capacity in the near future as demand skyrockets. One such approach has involved encoding data into strands of DNA—prior research has shown that it is possible. In the early stages of such research, scientists manually edited strands to add characteristics to represent zeroes or ones. More recently, researchers have used the CRISPR gene editing tool. Most such studies used DNA extracted from the tissue of deceased animals. More recently, researchers have begun efforts to move the research to living animals because it will last longer. And not just in the edited strands—the information they contain could conceivably be passed on to offspring, allowing data to be stored for very long periods of time.
Back in 2017, another team at Columbia University used CRISPR to detect a certain signal—in their case, it was the presence of sugar molecules. Adding such molecules resulted in gene expressions of plasmid DNA. Over time, the editing process was improved as genetic bits were added to represent ones and zeroes. Unfortunately, the system only allowed for storing a few bits of data.
Dr. Halima Benbouza is an Algerian scientist in the field of agronomic sciences and biological engineering.
She received her doctorate in 2004 from the University Agro BioTech Gembloux, Belgium studying Plant Breeding and Genetics and was offered a postdoctoral position to work on a collaborative project with the Agricultural Research Service, United States Department of Agriculture in Stoneville, Mississippi.
Subsequently, Dr. Benbouza was funded by Dow Agro Science to study Fusarium wilt resistance in cotton. In 2009 she was awarded the Special Prize Eric Daugimont et Dominique Van der Rest by the University Agro BioTech Gembloux, Belgium.
Dr. Benbouza is Professor at Batna 1 University where she teaches graduate and postgraduate students in the Institute of Veterinary Medicine and Agronomy. She also supervises Master’s and PhD students.
From 2010–2016, Dr. Benbouza served as inaugural Director of the Biotechnology Research Center (CRBt) in Constantine, appointed by the Ministry of Higher Education and Scientific Research. In 2011, she was appointed by the Algerian government as President of the Intersectoral Commission of Health and Life Sciences. Dr. Benbouza is a member of the Algerian National Council for Research Evaluation and a past member of the Sectorial Permanent Board of the Ministry of Higher Education and Scientific Research.
In 2013, Dr. Benbouza was appointed by the Prime Minister as President of the steering committee of Algeria’s Biotech Pharma project. In 2014 she was honored by the US Embassy in Algiers as one of the “Women in Science Hall of Fame” for her research achievements and her outstanding contribution to promote research activities and advance science in her country.
Aging is, at least for now, inevitable, and our eyes are not immune to those changes. Vision loss is, in fact, one of the top 10 causes of disability in the US., however, shows that this might be reversible in the future.
A large team of geneticists, ophthalmologists, and other scientists used a group of molecules called Yamanaka factors to turn cells in the eyes of mature mice back to a youthful state. This reversed the damage done by aging, and the cells were then able to regenerate, connect back to the brain, and vision was restored in both models of normal aging and glaucoma.
Yamanaka factors are nothing new in neuroscience. They are named after the after Shinya Yamanaka led research using those factors to convert mature adult cells back to stem cells, kickstarting the field of induced pluripotent stem cells — cells reprogrammed with the ability to generate other types of cells.
Scientists from the UCLA Jonsson Comprehensive Cancer Center have developed a simple, high-throughput method for transferring isolated mitochondria and their associated mitochondrial DNA into mammalian cells. This approach enables researchers to tailor a key genetic component of cells, to study and potentially treat debilitating diseases such as cancer, diabetes and metabolic disorders.
A study, published today in the journal Cell Reports, describes how the new UCLA-developed device, called MitoPunch, transfers mitochondria into 100000 or more recipient cells simultaneously, which is a significant improvement from existing mitochondrial transfer technologies. The device is part of the continued effort by UCLA scientists to understand mutations in mitochondrial DNA by developing controlled, manipulative approaches that improve the function of human cells or model human mitochondrial diseases better.
The ability to generate cells with desired mitochondrial DNA sequences is powerful for studying how genomes in the mitochondria and nucleus interact to regulate cell functions, which can be critical for understanding and potentially treating diseases in patients.
