Metformin has been proposed as an “anti-aging drug,” and a major clinical trial is about to get underway to test the idea.
New research from the University of California, Irvine, suggests aging is an important component of retinal ganglion cell death in glaucoma, and that novel pathways can be targeted when designing new treatments for glaucoma patients.
The study was published today in Aging Cell. Along with her colleagues, Dorota Skowronska‐Krawczyk, Ph.D., assistant professor in the Departments of Physiology & Biophysics and Ophthalmology and the faculty of the Center for Translational Vision Research at the UCI School of Medicine, describes the transcriptional and epigenetic changes happening in aging retina.
The team shows how stress, such as intraocular pressure (IOP) elevation in the eye, causes retinal tissue to undergo epigenetic and transcriptional changes similar to natural aging. And, how in young retinal tissue, repetitive stress induces features of accelerated aging including the accelerated epigenetic age.
Fasting database:
Recreates the immune system;…Prolonged fasting forces the body to use stores of glucose, fat and ketones, but it also breaks down a significant portion of white blood cells. Longo likens the effect to lightening a plane of excess cargo. During each cycle of fasting, this depletion of white blood cells induces changes that trigger stem cell-based regeneration of new immune system cells. In particular, prolonged fasting reduced the enzyme PKA, an effect previously discovered by the Longo team to extend longevity in simple organisms and which has been linked in other research to the regulation of stem cell self-renewal and pluripotency — that is, the potential for one cell to develop into many different cell types. Prolonged fasting also lowered levels of IGF-1, a growth-factor hormone that Longo and others have linked to aging, tumor progression and cancer risk.
Recreates the immune system (page loads slow)
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The company will also expend an aging Falcon 9 booster during a mission for the first time.
SpaceX aims to perform two Falcon 9 rocket launches only six hours apart after a mission scheduled for Nov. 21 was delayed, a report from Teslarati reveals.
A record-breaking year for SpaceX.
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A research team has identified a molecular target that could open up new therapeutic options to treat aging-associated diseases like Parkinson’s. Scientists at the University of Cologne have discovered how cells can eliminate mutated mitochondrial DNA (mtDNA). Mitochondria are the powerhouses of our cells. Due to their evolutionary descent from bacteria, they still have genetic material packaged in chromosome-like structures (nucleoids). They convert the chemical energy in our food into a biologically usable form. A team of researchers from the University of Cologne’s Physiology Centre at the Faculty of Medicine, the Centre for Molecular Medicine Cologne (CMMC) and the CECAD Cluster of Excellence for Aging Research has now shown that mutations of the mtDNA lead to a local rearrangement of proteins in the mitochondrial membrane. The mutated mtDNA is targeted, eliminated, and subjected to autophagy, the cellular ‘waste disposal’. The results have appeared in Nature Communications under the title ‘Mitochondrial membrane proteins and VPS35 orchestrate selective removal of mtDNA’.
In many tissues, mutations in mtDNA accumulate as a result of normal aging. These kinds of mutations are an important cause of many aging-associated diseases. There are thousands of copies mtDNA in every cell, so mitochondrial function is only impaired when the percentage of mutated mtDNA molecules exceeds a certain threshold value. It has long been established that mitochondrial damage, including acute mtDNA damage, triggers the process of mitophagy. In this process, dysfunctional mitochondrial parts are selectively degraded and recycled.
Dr David Pla-Martin, the lead author of the current study, explained the details: ‘What is new in our study is that this mechanism does not affect the cells’ endowment with mitochondria, but only clears out the damaged mtDNA. By labelling neighbouring proteins — so-called proximity labelling — we showed that mtDNA damage leads to the recruitment of endosomes in close proximity to nucleoids.’ Their removal is coordinated by the interaction of the nucleoid protein Twinkle and the mitochondrial membrane proteins SAMM50 and ATAD3 controls their distribution, SAMM50 induces the release and transfer of the nucleoid to the so-called endosomes. ‘This additionally prevents the activation of an immune response. The protein VPS35, the main component of the retromer, mediates the maturation of early endosomes into late autophagy vesicles, where degradation and recycling ultimately take place,’ said Pla-Martin.
Large language models have advanced significantly in recent years (LLMs). Impressive LLMs have been revealed one after the other, beginning with OpenAI’s GPT-3, which generates exceptionally correct texts and ends with its open-source counterpart BLOOM. Language-related problems that were previously unsolvable had become simply a challenge for these systems.
All of this progress is made possible by the vast amount of data available on the Internet and the accessibility of powerful GPUs. As appealing as they may sound, training an LLM is an incredibly expensive procedure in terms of both data and technology needs. We’re talking about AI systems with billions of parameters, so feeding these models with enough data isn’t easy. However, once you do it, they give you a stunning performance.
Have you ever wondered where the development of “computing” gadgets began? Why did individuals devote so much time and energy to designing and constructing the first computers? We can presume it was not for the purpose of amusing people with video games or YouTube videos.
Harvard University geneticist Dr. David Sinclair’s lab is developing a cheek swab test kit so that you can check your biological age at home. You then get updates on how to slow down and reverse your aging.
Find out how fast you’re aging with Tally Health. The future of healthy aging is here.
“A world without heart attack and stroke” — New video from our 2022 #RejuvenationStartupSummit: Mike Kope, CEO of Corporate Affairs, Cyclarity Therapeutics — prevents age-related conditions such as atherosclerosis, heart attack, and stroke by addressing the root cause. Enjoy!
Mike Kope, CEO of Cyclarity Therapeutics at Rejuvenation Startup Summit 2022.
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“Leveraging a platform to develop therapeutics that render calcified tissue and organs supple again” — New video from our #RejuvenationStartupSummit: Matthias Breugelmans, CEO of Elastrin Therapeutics Inc… Enjoy!
Matthias Breugelmans, CEO of Elastrin Therapeutics at Rejuvenation Startup Summit 2022.
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Scientists at Nanyang Technological University, Singapore (NTU Singapore) have found that a stress response in cells, when ‘switched on’ at a post-reproductive age, could be the key to slowing down aging and promoting longevity.
Longevity. Technology: In lab experiments on a type of roundworm that shares similarities with humans – paging C elegans – the NTU Singapore team found that switching on this stress response in aged worms by feeding them a high-glucose diet extended their lifespan as compared with worms fed a normal diet.
Publishing today in Nature Communications, the NTU team say this is the first time a link between this stress response and aging has been uncovered.
