August will see the second annual Longevity Summit take place in Dublin. Packed with keynote presentations by leading experts in the aging field, the summit will showcase some of the latest – and most exciting – research and innovations in the longevity space.
Earlier this week, we caught up with Dr de Grey to find out more about the conference, its speakers and agenda, and today we dig into what he and LEV Foundation have been up to.
Year 2014 face_with_colon_three Basically the whole bodies cells could be a pacemaker enabling even immortality with electricity at low voltage.
In pigs, scientists have succeeded in turning cardiac muscle cells into specialized pacemaker cells. Such technology could eventually replace electronic pacemakers, researchers say.
A study has found that a mitochondrial disease in newborns shows cancer-like changes in proliferating cells, causing tissues to age prematurely. The finding is a significant step forward in understanding the syndrome and developing treatments for mitochondrial diseases.
GRACILE syndrome, a mitochondrial disease that is one of the Finnish heritage diseases, shows altered cell metabolism and proliferation resembling that of cancer cells. In the future, similar mitochondrial diseases could potentially be treated by limiting excessive cell proliferation. This is demonstrated in a study led by docent Jukka Kallijärvi and professor emerita Vineta Fellman that was carried out at the Folkhälsan Research Center and the University of Helsinki and published in Nature Communications in April 2023.
Mitochondria are organelles responsible for a large portion of cellular energy metabolism. Mutations in genes required for mitochondrial functions cause mitochondrial diseases in humans. GRACILE syndrome is caused by a malfunction in the respiratory chain, the very system the mitochondria utilize to generate cellular energy. The onset of the syndrome is in the fetal period, manifesting after birth as a liver and kidney disease with severe metabolic complications. Newborns with the syndrome usually only survive a few weeks.
Our cells naturally degrade over time, which is part of the reason we’re not as mobile and sprightly aged 80 as we are aged 8. Now scientists have figured out a way to boost cell lifespan and longevity using a synthetic genetic ‘clock’.
Researchers from the University of California San Diego based their findings on the yeast Saccharomyces cerevisiae, making it unlikely that humans might live forever any time soon – but the team thinks that the work could be developed to eventually help the human body age in a healthier way.
By ‘rewiring’ the yeast cells, the researchers were able to boost their lifespan by 82 percent on average. It’s a promising development in the control of cellular aging and treating age-related conditions.
It works for retinitis pigmentosa (RP) and dry age-related macular degeneration (AMD).
Science Corp has conceived of a new bionic eye that targets and cures two diseases that cause blindness. “Today we’re excited to take the covers off of our first flagship product development program: the Science Eye, a visual prosthesis targeted at retinitis pigmentosa (RP) and dry age-related macular degeneration (AMD), two forms of serious blindness presently without good options for patients,” said the firm in a post from November 2022.
How does it work? By targeting the functioning of the diseases.
Peshkova/iStock.
“Today we’re excited to take the covers off of our first flagship product development program: the Science Eye, a visual prosthesis targeted at retinitis pigmentosa (RP) and dry age-related macular degeneration (AMD), two forms of serious blindness presently without good options for patients,” said the firm in a post from November 2022.
Scientists are still determining whether humans will reach a maximum possible age or if we can extend lifespan indefinitely. One thing we know is that the aging we see and feel in our bodies is connected to aging that individual cells experience. Yeast is a common model in molecular biology that is often used to study aging. In 2020, scientists found that yeast cells could go down one of two aging paths; in one, structures called nucleoli were degraded and ribosomal DNA experienced less silencing; in the other, mitochondria were affected and heme accumulation was reduced. The researchers suggested that these were two distinct types of terminal aging.
In follow-up work, the research team has manipulated the genetics of those pathways, and have extended the lifespan of cells by doing so. The work has been reported in Science. The investigators applied a solution to the cells that altered gene circuits to stop the cells from deteriorating.
Recently, a fake news article circulated the internet claiming that scientists had proven that stopping the ageing process was not possible. In this brief article, we explain why this claim is patently false and based entirely upon a wilful misinterpretation of scientific data.
It was an honor to speak at MIT’s Broad Institute about some of my past and present synthetic biology research on redesigning bacteria and viruses to act as delivery systems for biomedicine! Video recording is now available! Here is a link which should take you to 1:40:18 when my talk starts:[ ]. My talk was part of the inaugural MIT Biosummit (https://mitbiosummit.com/), a forward-looking conference which this year focused on tackling challenges at the interface of climate change and health sciences. #futureofmedicine #future #biotech #mit Thank you Ryan Robinson for helping to organize this conference and for giving your own excellent talk!
Recording of the MIT Club of Boston 2023 BioSummit: Human Health 2050 held at the Broad Institute on April 27, 2023. Note: Although the video is almost 6 hours long, you can rapidly navigate and skip to a particular speaker or session by scrubbing along the video timeline (in Chrome or Edge) or using the time markers listed below in blue (in all browsers). You can also use chapter browsing in the YouTube app on platforms where it is available.
Insulin-mTOR signaling drives anabolic growth in organismal development, while its late-life antagonistic pleiotropy affects aging and compromises lifespan across animal phylogeny. Here we identify LPD-3 as a megaprotein that orchestrates the tempo of insulin-mTOR signaling during C. elegans aging. We find that an agonist insulin INS-7 is drastically over-produced and shortens lifespan in lpd-3 mutants, a C. elegans model of human Alkuraya-Kučinskas syndrome. LPD-3 forms a bridge-like tunnel megaprotein to facilitate phospholipid trafficking to plasma membrane. Lipidomic profiling reveals increased abundance of hexaceramide species in lpd-3 mutants, accompanied by up-regulation of hexaceramide biosynthetic enzymes, including HYL-1 (Homolog of Yeast Longevity). Reducing HYL-1 activity decreases INS-7 levels and rescues the shortened lifespan of lpd-3 mutants through insulin receptor/DAF-2 and mTOR/LET-363. LPD-3 antagonizes SINH-1, a key mTORC2 component, and reduces protein abundance with age in wild type animals. We propose that LPD-3 acts as a megaprotein brake for aging and its age-dependent decline restricts lifespan through the sphingolipid-hexaceramide and insulin-mTOR pathways.
