Dialogues In Longevity With Dr. Aubrey de Grey, President & Chief Science Officer, Longevity Escape Velocity Foundation & Dr. Michael Rose, Director of the Network for Experimental Research on Evolution (NERE), and Professor, Department of Ecology and Evolutionary Biology, University of…
Aging reversed in dogs face_with_colon_three
Age-related decline in mobility and cognition are associated with cellular senescence and NAD+ depletion in dogs and people. A combination of a novel NAD+ precursor and senolytic, LY-D6/2 was examined in this randomized controlled trial. Seventy dogs were enrolled and allocated into placebo, low or full dose groups. Primary outcomes were change in cognitive impairment measured with the owner-reported Canine Cognitive Dysfunction Rating (CCDR) scale and change in activity measured with physical activity monitors. Fifty-nine dogs completed evaluations at the three-month primary endpoint, and 51 reached the six-month secondary endpoint. There was a significant difference in CCDR score across treatment groups from baseline to the primary endpoint (p=0.02) with the largest decrease in the full dose group. There were no significant differences between groups in changes in measured activity. However, the proportion of dogs that improved in frailty and owner-reported activity levels and happiness was higher in the full dose group than other groups. Adverse events occurred equally across groups. All groups showed improvement in cognition, frailty, and activity suggesting placebo effect and benefits of trial participation. We conclude that LY-D6/2 significantly improves owner-assessed cognitive function and may have broader effects on frailty, activity and happiness as reported by owners.
The authors have declared no competing interest.
Now in his 60s, the physician and entrepreneur is directing tens of millions of dollars at far-out tech to let him and others live twice as long, or longer.
The Forever Healthy Foundation is pleased to announce the Rejuvenation Startup Summit 2024 program and full speaker list.
The Rejuvenation Startup Summit (Berlin, May 10–11, 2024) is a vibrant networking event that brings together startups and members of the longevity venture capital/investor ecosystem – all aiming to create therapies to vastly extend the healthy human lifespan. Rejuvenation and longevity biotech is a new, emerging field of medicine. It aims to prevent and reverse the diseases of aging by addressing their common root cause, the aging process itself.
In addition to an exciting range of presentations from CEOs of startups in the fields of rejuvenation & longevity, the summit features an all-day startup forum for networking, panel discussions, and keynote presentations.
Dr. Dian Ginsberg presents what causes aging and successful cases of patients who shows DunedInPace of aging reduction by using a therapy in this video.
For More About Dr. Dian Ginsberg.
Website – Studies \& Researches.
https://www.youngplasmastudy.com/
https://dianginsbergmd.com/
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Perovskites, a broad class of compounds with a particular kind of crystal structure, have long been seen as a promising alternative or supplement to today’s silicon or cadmium telluride solar panels. They could be far more lightweight and inexpensive, and could be coated onto virtually any substrate, including paper or flexible plastic that could be rolled up for easy transport.
In their efficiency at converting sunlight to electricity, perovskites are becoming comparable to silicon, whose manufacture still requires long, complex, and energy-intensive processes. One big remaining drawback is longevity: They tend to break down in a matter of months to years, while silicon solar panels can last more than two decades. And their efficiency over large module areas still lags behind silicon.
Now, a team of researchers at MIT and several other institutions has revealed ways to optimize efficiency and better control degradation, by engineering the nanoscale structure of perovskite devices.
Half a century ago, scientists Jim Watson and Alexey Olovnikov independently realized that there was a problem with how our DNA gets copied. A quirk of linear DNA replication dictated that telomeres that protect the ends of chromosomes should have been growing shorter with each round of replication, a phenomenon known as the end-replication problem.
But a solution was forthcoming: Liz Blackburn and Carol Greider discovered telomerase, an enzyme that adds the telomeric repeats to the ends of chromosomes. “Case closed, everybody thought,” says Rockefeller’s Titia de Lange.
Now, research published in Nature suggests that there are two end-replication problems, not one. Further, telomerase is only part of the solution—cells also use the CST–Polα-primase complex, which has been extensively studied in de Lange’s laboratory.
The brain is typically depicted as a complex web of neurons sending and receiving messages. But neurons only make up half of the human brain. The other half—roughly 85 billion cells—are non-neuronal cells called glia.
The most common type of glial cells are astrocytes, which are important for supporting neuronal health and activity. Despite this, most existing laboratory models of the human brain fail to include astrocytes at sufficient levels or at all, which limits the models’ utility for studying brain health and disease.
Now, Salk scientists have created a novel organoid model of the human brain—a three-dimensional collection of cells that mimics features of human tissues—that contains mature, functional astrocytes. With this astrocyte-rich model, researchers will be able to study inflammation and stress in aging and diseases like Alzheimer’s with greater clarity and depth than ever before.
The leading networking event for rejuvenation startups, longevity investors, and translational researchers.
We conducted a multicenter, nested case–control study of Alzheimer’s disease biomarkers in cognitively normal participants who were enrolled in the China Cognition and Aging Study from January 2000 through December 2020. A subgroup of these participants underwent testing of cerebrospinal fluid (CSF), cognitive assessments, and brain imaging at 2-year–to–3-year intervals. A total of 648 participants in whom Alzheimer’s disease developed were matched with 648 participants who had normal cognition, and the temporal trajectories of CSF biochemical marker concentrations, cognitive testing, and imaging were analyzed in the two groups.
The median follow-up was 19.9 years (interquartile range, 19.5 to 20.2). CSF and imaging biomarkers in the Alzheimer’s disease group diverged from those in the cognitively normal group at the following estimated number of years before diagnosis: amyloid-beta (Aβ)42, 18 years; the ratio of Aβ42 to Aβ40, 14 years; phosphorylated tau 181, 11 years; total tau, 10 years; neurofilament light chain, 9 years; hippocampal volume, 8 years; and cognitive decline, 6 years. As cognitive impairment progressed, the changes in CSF biomarker levels in the Alzheimer’s disease group initially accelerated and then slowed.
In this study involving Chinese participants during the 20 years preceding clinical diagnosis of sporadic Alzheimer’s disease, we observed the time courses of CSF biomarkers, the times before diagnosis at which they diverged from the biomarkers from a matched group of participants who remained cognitively normal, and the temporal order in which the biomarkers became abnormal. (Funded by the Key Project of the National Natural Science Foundation of China and others; ClinicalTrials.gov number, NCT03653156. opens in new tab.)
