Experiments found increased lifespans and markers of health in mice, worms, and rhesus monkeys given supplemental taurine.
Category: life extension – Page 107
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A quarter-century ago, researchers discovered that adults, not just developing infants, can generate new brain cells, a process called neurogenesis. But it’s still not clear what role these new neurons play in health or disease.
In a new mouse study, Columbia University researchers found that neurogenesis in adults is critical for maintaining brain circuits that support working memory across the lifespan and chronic loss of adult neurogenesis causes progressive memory loss, like that seen in age-related cognitive decline and Alzheimer’s disease in humans.
The study, “Adult-born neurons maintain hippocampal cholinergic inputs and support working memory during aging,” was published in July in the journal Molecular Psychiatry.
Central learning and memory hubs change in response to sex hormones. A new study in Nature Mental Health by Rachel Zsido and Julia Sacher of the Max Planck Institute for Human Cognitive and Brain Sciences and the University Clinic in Leipzig, Germany, links rhythmic oscillations in ovarian hormone levels in women during the menstrual cycle to changes in brain structure.
Ovarian hormones have significant effects on the brain, and early menopause may be associated with an increased risk of accelerated brain aging and dementia later in life. However, the effects of ovarian hormone fluctuations on brain structure earlier in life are less defined. In their current study, Zsido and Sacher show that fluctuations in ovarian hormones affect structural plasticity in key brain regions during the reproductive years.
To do this, the scientists collected blood samples from 27 female study participants, used ultrasound to track follicle growth in the ovaries to pinpoint ovulation timing, and utilized ultra-high field 7 Tesla MRI to zoom into subregions of the medial temporal lobe and hippocampus. That’s because these regions are dense with sex hormone receptors and are critical for cognitive function, such as episodic memory.
Of the three great Stoics, Seneca always interested me the least. A playwright and professional philosopher, he seemed unlikely to be acquainted with the more mundane forms of suffering that beset humanity. This made him seem unfit to propound upon a philosophy concerned with right conduct under challenging circumstances.
Marcus Aurelius, ruler of an enormous empire, spent most of his reign embroiled in wars he had no desire to fight. Epictetus, a Greek who endured the hardships of slavery, also embodied the Stoic ideal. Cries of “ad hominem!” aside, it is hard to dispute that our experiences shape our outlooks on living. Biographical criticisms can be flimsy, but the central argument in De Brevitate Vitae — an otherwise inspirational classic — was exceptionally naive for the 1st century.
Although Seneca understood intrigue and exile firsthand, he was not privy to the time-sapping vicissitudes of householding or holding down a job.
How we grow old gracefully—and whether we can do anything to slow down the process—has long been a fascination of humanity. However, despite continued research the answer to how we can successfully combat aging still remains elusive.
Working with non-human primates, scientists have discovered that the protein SIRT2, a member of the sirtuin family, might play an important role in slowing cardiac aging [1].
In this study published in Nature Aging, the researchers used long-tailed macaques to elucidate the molecular aspects of cardiac aging using multi-omics analysis. Unlike short-lived mice and rats, non-human primates like these have hearts that closely resemble those of humans and, due to their relatively long lifespan, suffer from spontaneous heart conditions as well.
When it comes to human longevity, you might envision nanobots helping our bodies operate more efficiently. But our bodies are biological machines in their own right, evolved to handle any situation in the real world from illness to cold to hunger. Our bodies heal themselves, and they can be programmed to do so if we understood that language better.
This video talks about DNA and genes, and the epigenetic mechanisms that read that information. The epigenetic clock is one way to measure the age of cells, and this can be reversed with current technologies. We discuss experiments by David Sinclair, which made blind mice see again, and experiments by Greg Fahy, which regenerated the immune system of humans and reset their cellular age by 2 years.
Asking our bodies to heal themselves could be one of the largest medical breakthroughs ever, instead of trying mainly chemical means of medication. And it has significant implications for whether or not we can achieve longevity escape velocity and continue to live more or less indefinitely. This promises to be a very interesting topic.
#aging #longevity #science.
The science of super longevity | Dr. Morgan Levine.
https://www.youtube.com/watch?v=B_CqKVU19ec.
Groundbreaking Research on Anti-Aging: Unlock the Secrets to Longevity | David Sinclair.
Researchers at the University of Auckland identify platelet factor 4 (PF4) in young blood as a key player in reversing age-related cognitive decline in mice. The study offers a promising avenue for treating dementia-related conditions and enhancing brain function in aging populations.
Researchers developed ‘HistoAge,’ an algorithm that unravels brain aging and neurodegenerative disorders.
As we age, our brains undergo structural and cellular changes influenced by intrinsic and external factors. Accelerated aging in the brain can result in an increased risk of neurodegenerative conditions, bipolar disorder, and mortality. In a bid to deeply understand how an aging brain works, researchers say they have built a powerful AI tool that can identify regions in the brain vulnerable to age-related changes.
The team used AI to develop an algorithm called ‘HistoAge,’ which predicts age at death based on the cellular composition of human brain tissue specimens with an average accuracy… More.
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