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Japanese researchers are making groundbreaking discoveries on the mechanisms of aging and working to apply them. As we age, senescent cells, or aged cells that have stopped dividing, accumulate, causing inflammation that can damage blood vessels and organs. Animal experiments have shown that removing these cells improves kidney function and reduces arteriosclerosis. They have led to the identification of a drug and development of a vaccine to eliminate the cells.

Disrupted sleep-wake and molecular circadian rhythms are a feature of aging associated with metabolic disease and reduced levels of NAD+, yet whether changes in nucleotide metabolism control circadian behavioral and genomic rhythms remains unknown. Here, we reveal that supplementation with the NAD + precursor nicotinamide riboside (NR) markedly reprograms metabolic and stress-response pathways that decline with aging through inhibition of the clock repressor PER2. NR enhances BMAL1 chromatin binding genome-wide through PER2 K680 deacetylation, which in turn primes PER2 phosphorylation within a domain that controls nuclear transport and stability and that is mutated in human advanced sleep phase syndrome.

Scientists created a stem cell-based method to produce high-quality mitochondria at scale, enabling effective treatments for osteoarthritis and other diseases linked to mitochondrial dysfunction. Scientists have developed a groundbreaking method to mass-produce high-quality human mitochondria, a

In humans and other multicellular organisms, cells multiply. This defining feature allows embryos to grow into adulthood, and enables the healing of the many bumps, bruises and scrapes along the way.

Certain factors can cause cells to abandon this characteristic and enter a zombie-like state known as senescence where they persist but no longer divide to make new cells. Our bodies can remove these senescent cells that tend to pile up as we age. The older we get, however, the less efficient our immune systems become at doing so.

“In addition to no longer growing and proliferating, the other hallmark of senescent cells is that they have this inflammatory program causing them to secrete inflammatory molecules,” said Peter Adams, Ph.D., director and professor of the Cancer Genome and Epigenetics Program at Sanford Burnham Prebys and senior and co-corresponding author of the study.

Professor Kenji Osafune (Department of Cell Growth and Differentiation) and his team of researchers have devised an effective means to grow iPS cell-derived kidney progenitor cells, paving the way for renal regenerative therapies to become a reality. The findings are published in the journal Science Translational Medicine.

Modern medicine continues to be hampered by the lack of effective treatments for (AKI) and (CKD). Regenerative medicine, such as cell replacement therapies, represents a new hope for patients. Yet, such therapeutic approaches require large-scale production of the necessary cells, which had remained a challenge until this discovery.

Using a mouse model of AKI, the research team first demonstrated the therapeutic potential of human iPS cell-derived nephron progenitor cells (hiPSC-NPCs). When these cells were transplanted into the kidneys of AKI mouse models induced by an anti-cancer drug, cisplatin, the animals’ survival was vastly improved by preventing the deterioration of kidney function.

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Brigham and Women’s Hospital-led research reports no significant long-term benefit of cocoa flavanol supplementation in preventing age-related macular degeneration (AMD). The paper is published in the journal JAMA Ophthalmology.

AMD is a progressive retinal disease and the most common cause of severe vision loss in adults over age 50. AMD damages the macula, the central part of the retina responsible for sharp, detailed vision. While peripheral sight is typically preserved, central vision loss can impair reading, driving, facial recognition, and other quality of life tasks. Abnormalities of blood flow in the eye are associated with the occurrence of AMD.

Cocoa flavanols are a group of naturally occurring plant compounds classified as flavonoids, found primarily in the cocoa bean. These bioactive compounds have been studied for their vascular effects, including improved endothelial function and enhanced nitric oxide production, which contribute to vasodilation and circulatory health. Previous trials have shown that moderate intake of may , improve lipid profiles, and reduce markers of inflammation, suggesting a role in mitigating cardiovascular and related vascular conditions.

Could Short Chains of Amino Acids Revolutionize Anti-aging? We explore the exciting potential of peptide therapy to address key hallmarks of aging, including biological age and telomere length. This video delves into the science behind peptides and examines early clinical findings that suggest significant possibilities for age reversal.

What you’ll learn:
• Key peptides being studied for anti-aging (Epitalon, GHK-Cu, etc.).
• A look at clinical studies and patient data.
• The future of peptide therapy in longevity research.

Credits to : glycanage, dr. luis martinez of clinical peptide society

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Researchers harness the power of the world’s most advanced supercomputers to simulate the inner workings of cellular machinery that repairs DNA and helps prevent life-threatening diseases. Sunburn and premature aging are well-known consequences of exposure to ultraviolet (UV) radiation, tobacco s

In a study in aging mice, the first author has uncovered striking age-related changes in the sugary coating – called the glycocalyx – on cells that form the blood-brain barrier, a structure that protects the brain by filtering out harmful substances while allowing in essential nutrients.

“The glycocalyx is like a forest,” the author explains. “In young, healthy brains, this forest is lush and thriving. But in older brains, it becomes sparse, patchy, and degraded.”

These age-related changes to the glycocalyx weaken the blood-brain barrier, the author found. As the barrier becomes leaky with age, harmful molecules can infiltrate the brain, potentially fueling inflammation, cognitive decline, and neurodegenerative diseases.

The results were striking: In older mice, bottlebrush-shaped, sugar-coated proteins called mucins, a key component of the glycocalyx, were significantly reduced. This thinning of the glycocalyx correlated with increased permeability of the blood-brain barrier and heightened neuroinflammation.

When the team reintroduced those critical mucins in aged mice, restoring a more “youthful” glycocalyx, they improved the integrity of the blood-brain barrier, reduced neuroinflammation, and measurably improved cognitive function.

“Modulating glycans has a major effect on the brain – both negatively in aging, when these sugars are lost, and positively, when they are restored,” the lead says. “This opens an entirely new avenue for treating brain aging and related diseases.”