Vaccines may do far more than prevent infections.
The way that some inoculations train your immune system could also reduce the risk of cancer, stroke, or heart attacks, and possibly guard against dementia.
New evidence shows that the shingles vaccine is linked to slower aging, with benefits that can last for several years after vaccination.
Researchers at the Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine), have found that a key protein can help to regenerate neural stem cells, which may improve aging-associated decline in neuronal production of an aging brain.
Published in Science Advances, the study identified a transcription factor in the brain, cyclin D-binding myb-like transcription factor 1 (DMTF1), as a critical driver of neural stem cell function during the aging process. Transcription factors are proteins that regulate genes to ensure that they are expressed correctly in the intended cells.
The study, led by Assistant Professor Ong Sek Tong Derrick and first author Dr. Liang Yajing, both from the Department of Physiology and the Healthy Longevity Translational Research Program at NUS Medicine, sought to identify biological factors that influence the degeneration of neural stem cell function often associated with aging, and guide the development of therapeutic approaches to mitigate the adverse effects of neurological aging.
Ray, you’ve made two predictions that I think are important. The first one, as you said, was the one you announced back in 1989: that we would reach human-level AI by 2029. And as you said, people laughed at it.
But there’s another prediction you’ve made: that we will reach the Singularity by 2045. There’s a lot of confusion here. In other words, if we reach human-level AI by 2029 and it then grows exponentially, why do we have to wait until 2045 for the Singularity? Could you explain the difference between these two?
It’s because that’s the point at which our intelligence will become a thousand times greater. One of the ways my view differs from others is that I don’t see it as us having our own intelligence—that is, biological intelligence—while AI exists somewhere else, and we interact with it by comparing human intelligence to AI.
Founder of XPRIZE and pioneer in exponential technologies. Building a world of Abundance through innovation, longevity, and breakthrough ventures.
Over 60? THIS Morning Habit TRIPLES Stroke Risk In Older Adults! | Senior Health Tips.
Most people don’t know this, but the first 90 minutes after waking are the most dangerous for adults over 60 — especially when it comes to stroke risk. 🧠⚠️ New studies from Harvard, Tokyo, and Toronto reveal that certain common morning habits can dramatically increase vascular stress, spike blood pressure, restrict blood flow to the brain, and trigger dangerous clotting patterns in older adults. These habits look harmless on the outside, but inside the body, they create the perfect storm for a stroke. 😳
In this video, we reveal the 6 morning habits that triple stroke risk in seniors, ranked from least to most dangerous. You’ll learn why the aging vascular system reacts differently in the morning, why certain actions overload the arteries, how sudden pressure changes affect the brain, and the specific morning routines neurologists now warn older adults to avoid. We also explain what the research discovered about Habit #1 — a behavior so strongly linked to stroke risk that scientists repeated the study twice to confirm the results. 🧬📊
If you or someone you love is over 60, this is essential information. These morning habits can quietly raise your risk without symptoms, but the good news is that simple changes can help protect your brain, improve circulation, and lower your chances of experiencing a life-altering event. ❤️🩹 Stay until the end — your brain health may depend on it.
⌛Timestamps:
⏱️ Intro – 00:00
⚠️ Habit No.5 – 02:36
⚠️ Habit No.4 – 05:57
⚠️ Habit No.3 – 09:24
⚠️ Habit No.2 – 13:30
⚠️ Habit No.1 – 17:54
#SeniorHealth #SeniorHealthTips #SeniorWellness #SeniorZone #StrokeRisk #StrokePrevention #MorningHabits #Over60Health #BrainHealth #HealthyAging #SeniorSafety #HighBloodPressure #CirculationHealth #AgingWell #UnitedStates #Wisdom #NeurologyTips #SeniorCare #VascularHealth #HealthyMorningRoutine #LongevityTips.
Ray Kurzweil predicts humans will merge with artificial intelligence (AI) by 2045, resulting in a 1000x increase in intelligence and marking the beginning of a new era of unprecedented innovation, potentially transforming human life and society ## ## Questions to inspire discussion.
Preparing for AI Timeline.
🤖 Q: When should I expect human-level AI and what defines it? A: Human-level AI arrives by 2029, defined not by passing the Turing test (which only matches an ordinary person), but as AGI requiring expertise in thousands of fields and the ability to combine insights across disciplines.
🧠 Q: When will the singularity occur and what intelligence gain can I expect? A: The singularity happens by 2045 when humanity merges with AI to become 1000x more intelligent, creating a seamless merger where biological and computational thought processes become indistinguishable.
⚡ Q: How much change should I prepare for in the next decade? A: Expect as much change in the next 10 years as occurred in the last 100 years (1925−2025), with AGI and supercomputers by 2035 enabling merging with AI for 1000x intelligence increase.
Career and Economic Adaptation.
Early diagnosis and noninvasive monitoring of neurological disorders require sensitivity to elusive cellular-level alterations that emerge much earlier than volumetric changes observable with millimeter-resolution medical imaging.
Morphological changes in axons—the tube-like projections of neurons that transmit electrical signals and constitute the bulk of the brain’s white matter—are a common hallmark of a wide range of neurological disorders, as well as normal development and aging.
A study from the University of Eastern Finland (UEF) and the New York University (NYU) Grossman School of Medicine establishes a direct analytical link between the axonal microgeometry and noninvasive, millimeter-scale diffusion MRI (dMRI) signals—diffusion MRI measures the diffusion of water molecules within biological tissues and is sensitive to tissue microstructure.
In a surprising discovery, University of New Mexico researchers have found that OTULIN – an enzyme that helps regulate the immune system – also drives the formation of tau, a protein implicated in many neurodegenerative diseases, as well as brain inflammation and aging.
In a study published in the journal Genomic Psychiatry, the researchers reported that when they deactivated OTULIN, either by administering a custom-designed small molecule or knocking out the gene that codes for it, it halted the production of tau and removed it from neurons. The study was conducted on two different types of cells, some derived from a patient who had died from late-onset sporadic Alzheimer’s disease, and the rest from a line of human neuroblastoma cells that are frequently used in neuroscience research.
The discovery opens the door to potential treatments for Alzheimer’s and other neurodegenerative diseases, said Karthikeyan Tangavelou, PhD, a senior scientist in the lab of Kiran Bhaskar, PhD, professor in the Department of Molecular Genetics & Microbiology in the UNM School of Medicine.
Significance.
Cellular rejuvenation through transcriptional reprogramming has emerged as exciting approach to counter aging. However, to date, only a few of rejuvenating transcription factor (TF) perturbations have been identified. In this work, we developed a discovery platform to systematically identify single TF perturbations that drive cellular and tissue rejuvenation. Using a classical model of human fibroblast aging, we identified more than a dozen candidate TF perturbations and validated four of them (E2F3, EZH2, STAT3, ZFX) through cellular/molecular phenotyping. At the tissue level, we demonstrate that overexpression of EZH2 alone is sufficient to rejuvenate the liver in aged mice, significantly reducing fibrosis and steatosis, and improving glucose tolerance. Our work expanded the list of candidate rejuvenating TFs for future translation. Abstract.
Cellular rejuvenation through transcriptional reprogramming is an exciting approach to counter aging. Using a fibroblast-based model of human cell aging and Perturb-seq screening, we developed a systematic approach to identify single transcription factor (TF) perturbations that promote rejuvenation without dedifferentiation. Overexpressing E2F3 or EZH2, and repressing STAT3 or ZFX, reversed cellular hallmarks of aging—increasing proliferation, proteostasis, and mitochondrial activity, while decreasing senescence. EZH2 overexpression in vivo rejuvenated livers in aged mice, reversing aging-associated gene expression profiles, decreasing steatosis and fibrosis, and improving glucose tolerance. Mechanistically, single TF perturbations led to convergent downstream transcriptional programs conserved in different aging and rejuvenation models. These results suggest a shared set of molecular requirements for cellular and tissue rejuvenation across species. Sign up for PNAS alerts.
Get alerts for new articles, or get an alert when an article is cited. Cellular rejuvenation through transcriptional reprogramming is an exciting approach to counter aging and bring cells back to a healthy state. In both cell and animal aging models, there has been significant recent progress in rejuvenation research. Systemic factors identified in young blood through models such as heterochronic parabiosis (in which the circulatory systems of a young and aged animal are joined) rejuvenate various peripheral tissues and cognitive function in the brain (1–4). Partial reprogramming at the cellular level with the Yamanaka factors (four stem cell transcription factors) reverses cellular and tissue-level aging markers and can extend lifespan in old mice (5–8). These discoveries support the notion that transcriptional reprogramming is a powerful approach to improving the health of cells and tissues, and one day could be used as an approach for human therapeutics. However, to date, only a couple of rejuvenating transcription factor (TF) perturbations have been identified (9, 10) and most of them require the overexpression of TFs. We hypothesized that there are multiple other TF perturbations which could reset cells and tissues back to a healthier or younger state—rejuvenating them. Identifying complementary rejuvenating strategies is important as it will increase the chance of successful future translation. We developed a high-throughput platform, the Transcriptional Rejuvenation Discovery Platform (TRDP), which combines computational analysis of TF binding motifs and target predictions (Materials and Methods), global gene expression data of old and young cell states, and experimental genetic perturbations to identify which TF can restore overall gene expression and cell phenotypes to a younger, healthier state. We developed TRDP to be applicable to any cell type, and in both aging and disease settings, with the only requirements being baseline comparison of gene expression data comparing the older/diseased state to the younger/healthier state and the ability to perform genetic perturbations. To model aging in vitro as a validation of our approach, we used the canonical aging model of passaged fibroblasts (11, 12). We tested 400 TF perturbations via our screen and validated reversal of key cellular aging hallmarks in late passage human fibroblasts for four top TFs: E2F3, EZH2, STAT3, and ZFX. Moreover, EZH2 overexpression in vivo rejuvenated livers in aged mice—reversing aging-associated global gene expression profiles, significantly reducing steatosis and fibrosis, and improving glucose tolerance. These findings point to a conserved set of molecular requirements for cellular and tissue rejuvenation.
We sit down with José Cordeiro, author of The Death of Death, to uncover the timeline scientists believe could end aging — and even achieve immortality. From the promise of longevity escape velocity by 2030 to Ray Kurzweil’s bold prediction of immortality by 2045, José reveals the breakthroughs, roadblocks, and revolutionary ideas shaping the future of human life.
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