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.
As one of the OMICS in systems biology, metabolomics defines the metabolome and simultaneously quantifies numerous metabolites that are final or intermediate products and effectors of upstream biological processes. Metabolomics provides accurate information that helps determine the physiological steady state and biochemical changes during the aging process. To date, reference values of metabolites across the adult lifespan, especially among ethnicity groups, are lacking. The “normal” reference values according to age, sex, and race allow the characterization of whether an individual or a group deviates metabolically from normal aging, encompass a fundamental element in any study aimed at understanding mechanisms at the interface between aging and diseases.
A recent study demonstrated that non-invasive stimulation of the right cerebellum led to improvements in episodic memory performance in healthy elderly individuals, at the end of a 12-day neurostimulation program, and also at the point of a 4-month follow-up.
The steady increase in average life expectancy poses significant challenges to individuals, families, and societies across multiple dimensions. Estimating that by 2050 one in every six individuals will be over the age of 65, the study of aging and its association with cognitive decline, neurodegenerative diseases and overall frailty is becoming increasingly important.
Therefore, it has been an important goals of neurosciences research to understand the relationship between the aging brain and episodic memory deficits and to develop interventions to mitigate the age-related decline in our ability to remember personal past events (episodic memory).
