Lifeboat Foundation

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.

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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.)

We are all ultimately overtaken by age, yet for some people, the correct genes can make the journey into old age rather slow.

Italian researchers made a unique discovery regarding people who survive well into their 90s and beyond a few years ago: they frequently possess a variant of the gene BPIFB4 that guards against cardiovascular disease and maintains the heart in excellent condition for a longer period of time.

Science and Technology: I don’t want to die.

A friend of the academic, who died in the US in 2021, says his brain has been cryonically preserved in accordance with his final wishes.

We don’t exactly know why we age; we know what aging looks like —the “symptoms”, so to speak— but the root causes remain foggy. One leading hypothesis is that the changes associated with old age, both external and internal, are a result of accumulating DNA damage. As this damage builds, cellular functions begin to break down and important pathways start going haywire.

One of the most extreme forms of DNA damage is the double-strand break, which happens when a strand of DNA snaps in half, leaving two separate slivers floating around. Left unfixed, these strands can snag at and break chromosomes, leading to diseases like cancer and other disorders. But how the body repairs this kind of wreckage has been a source of mystery. Now, scientists at the Dresden University of Technology have managed to shine a light on the process. Published in Cell, their work offers important new insights that may eventually help treat, and possibly reverse, DNA damage.

The capacity of intestinal stem cells to maintain cellular balance in the gut decreases upon ageing. Researchers at the University of Helsinki have discovered a new mechanism of action between the nutrient adaptation of intestinal stem cells and ageing. The finding may make a difference when seeking ways to maintain the functional capacity of the ageing gut.

The cellular balance of the intestine is carefully regulated, and it is influenced, among other things, by nutrition: ample nutrition increases the total number of cells in the gut, whereas fasting decreases their number.

The relative number of different types of cells also changes according to nutrient status.

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