For decades, scientists have focused on amyloid plaques—abnormal clumps of misfolded proteins that accumulate between neurons—as a therapeutic target for Alzheimer’s disease. But anti-amyloid therapies haven’t made strong headway in treating the devastating condition.
Now, researchers at Yale School of Medicine (YSM) are zeroing in on a byproduct of these plaques, called axonal spheroids, and exploring how to reverse their growth. They published their findings March 10 in Nature Aging.
Axonal spheroids are bubble-like structures on axons—the part of the neuron that sends messages through electrical impulses—that form due to swelling induced by amyloid plaques. Previous research at YSM has shown that as these spheroids grow, they block electricity conduction in the axons, which can hinder the ability to communicate with other neurons.
As Shakespeare put it, we all have our entrances and our exits on this grand stage we call life, and now researchers have identified the specific point in middle-age when our brain cells show the first signs of starting down a downward slope.
That age, based on brain scans and tests covering 19,300 individuals, is on average around 44 years. It’s here that degeneration starts to be noticeable, before hitting its most rapid rate at age 67. By the time we reach 90, the speed of brain aging levels off.
According to the team behind the new study, led by researchers from Stony Brook University in the US, the findings could be helpful in figuring out ways to promote better brain health during the later stages of life.
Dissecting the effects of hypothermic and hypometabolic states on aging processes, the authors show that activation of neurons in the preoptic area induces a torpor-like state in mice that slows epigenetic aging and improves healthspan. These pro-longevity effects are mediated by reduced Tb, reinforcing evidence that Tb is a key mediator of aging processes.
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Regular use of math and reading skills could prevent cognitive decline with age, according to a new Science Advances study.
Cognitive skills of the population such as literacy and numeracy are important not only for individual incomes but also for the economic growth of nations (2–6). As a result, the aging of world populations presents an economic concern if the commonly assumed declines of these skills with age hold.
We use longitudinal variation in individual literacy and numeracy skills for a representative adult sample to create age-skill profiles that credibly separate age from cohort effects. The pure age component that we derive provides a different perspective on the impacts of aging populations. Overall, our results are not consistent with a view that a natural law dictates an inevitable decline in these skills with age. Potential cognitive declines only occur at later ages and are not inevitable with usage of skills.
This is consolation for countries with aging populations, but avoidance of skill losses is not automatic and appears related to stimulation from skill usage. These results thus suggest that age-skill relationships of adults deserve policy attention, consistent with concerns about the necessity of lifelong learning.
Centenarians, once considered rare, have become commonplace. Indeed, they are the fastest-growing demographic group of the world’s population, with numbers roughly doubling every ten years since the 1970s.
How long humans can live, and what determines a long and healthy life, have been of interest for as long as we know. Plato and Aristotle discussed and wrote about the ageing process over 2,300 years ago.
The pursuit of understanding the secrets behind exceptional longevity isn’t easy, however.
“The Future of Human Evolution: AI, Genetic Engineering, and the Rise of Post-Human Civilization”
What happens when human evolution is no longer shaped by nature but by artificial intelligence and genetic engineering? This story explores the rise of AI-enhanced humans in a futuristic medieval world, where the fusion of bioengineering, AI consciousness, and neural implants creates a post-human era. As civilizations embrace transhumanism, traditional humanity faces extinction, replaced by a new species of synthetic life. Will this AI-driven society achieve ultimate enlightenment, or will it lose the essence of what makes us human? The battle between future civilization, advanced technology, and those clinging to the past intensifies as digital immortality reshapes the meaning of existence. This cybernetic future forces us to question our identity—can genetic modification and AI singularity coexist with the soul of humanity? Witness the evolution of intelligence, the struggle between AI vs humanity, and the uncertain fate of a world where consciousness itself is no longer biological.
0:00 — Introduction: The Future of Human Evolution. 8:25 — AI & Genetic Engineering: Unlocking Human Potential. 16:50 — Ethical Dilemmas of Genetic Modification. 25:15 — The Rise of Engineered Intelligence. 33:40 — Genetic Enhancements & Social Stratification. 42:05 — AI in Education, Work, and Society. 50:30 — The Quest for Longevity & Immortality. 58:55 — Resistance Movements Against Enhancement. 1:07:20 — The First AI-Integrated Humans. 1:15:45 — The Breakdown of Traditional Humanity. 1:24:10 — Post-Human Civilizations & Digital Consciousness. 1:32:35 — The Divide Between Organic & Artificial Life. 1:41:00 — The Singularity & The End of Natural Evolution. 1:49:25 — What Comes After Humanity?
Sources. Bostrom, N. (2014). Superintelligence: Paths, Dangers, Strategies. Oxford University Press. Harari, Y. N. (2017). Homo Deus: A Brief History of Tomorrow. Harper. Kurzweil, R. (2005). The Singularity Is Near: When Humans Transcend Biology. Penguin. Tegmark, M. (2017). Life 3.0: Being Human in the Age of Artificial Intelligence. Knopf. Goertzel, B. (2020). Artificial General Intelligence: Concept, State of the Art, and Future Directions. Springer.
Transiently reprogramming human fibroblasts up to the maturation phase rejuvenates cells according to several aging markers whilst enabling them to return to their original identity.
In this edition, we’ll take a look at a Canadian study which shows that reducing a worm’s ability to fight free radicals in a specific organ could increase it’s lifespan. Does this have any implications for humans?
Contents:
Intro 0:00 Graphical Abstract 1:49 Figure 1. Tissue-specific re-expression of sod-2 rescues deficits in fertility and embryonic lethality in clk-1;sod-2 mutants 2:28 Figure 2. Tissue-specific re-expression of sod-2 can decrease stress resistance in clk-1;sod-2 worms 5:37 Figure 3. Tissue-specific re-expression of sod-2 is not sufficient to reduce clk-1;sod-2 lifespan 6:41 Figure 4. Disruption of mitochondrial superoxide dismutase in the intestine is sufficient to increase lifespan 7:33 Figure 5. Intestine-specific knockdown of sod-2 is sufficient to enhance resistance to heat stress 9:33 Figure 6. Intestine-specific knockdown of sod-2 does not affect physiologic rates 10:29 Conclusion & Next Steps 11:40
