A study of 86,000 adults across Europe links multilingualism to slower biological aging. Researchers found that people who speak multiple languages tend to maintain better cognitive function and physical health than their monolingual peers.
Category: life extension
Metformin: decelerates biomarkers of aging clocks
Signal Transduction and Targeted Therapy volume 9, Article number: 319 (2024) Cite this article.
Dr. Chris Oswald — Precision Nutrition, Epigenetics & Practitioner-Led Longevity Care
Precision Nutrition, Epigenetics & Practitioner-Led Longevity Care — Dr. Chris Oswald — Head of Medical Affairs, Pure Encapsulations, Nestlé Health Science.
Dr. Chris Oswald, DC, CNS, is Head of Medical Affairs for Pure Encapsulations (https://www.pureencapsulations.com/), part of Nestlé Health Science family. He is a chiropractor, certified nutrition specialist and certified functional medicine practitioner and has been treating patients since 2007.
At Pure Encapsulations, Dr. Oswald leads medical education, scientific strategy, and innovation across well-known professional brands including Pure Encapsulations, Douglas Labs, Klean Athlete, Genestra, and others. In this role, he sits at the intersection of clinical science, practitioner education, and product innovation — translating complex evidence into practical tools that help healthcare professionals practice more confident, personalized nutritional medicine.
Dr. Oswald’s clinical work, in combination with his work in professional dietary supplement companies, gives him unique insight into the creation of clinically useful tools and education to support the unique needs of clinicians and patients in functional, integrative and natural health.
Before joining Pure Encapsulations, Dr. Oswald held senior leadership roles across the nutraceutical and health tech landscape, including Chief Science Officer, Head of Product Innovation and R&D, Head of Operations, Interim Head of Sales, and VP of Nutraceuticals at companies like January AI and Further Food. Across those roles, he’s led everything from supply chain and regulatory strategy to product development, claims substantiation, and national practitioner education.
Sprint or marathon? Aging muscle stem cells shift from rapid repair to long-term survival
Aging muscles heal more slowly after injury—a frustrating reality familiar to many older adults. A UCLA study conducted in mice reveals an unexpected cause: Stem cells in aged muscle accumulate higher levels of a protein that slows their ability to activate and repair tissue, but helps the cells survive longer in the harsh environment of aging tissue.
The findings, published today in the journal Science, suggest that some molecular changes associated with getting older may actually be protective adaptations rather than purely detrimental effects.
“This has led us to a new way of thinking about aging,” said Dr. Thomas Rando, senior author of the new study and director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.
Cellular survivorship bias as a mechanistic driver of muscle stem cell aging
Aging is characterized by a decline in the ability of tissue repair and regeneration after injury. In skeletal muscle, this decline is largely driven by impaired function of muscle stem cells (MuSCs) to efficiently contribute to muscle regeneration. We uncovered a cause of this aging-associated dysfunction: a cellular survivorship bias that prioritizes stem cell persistence at the expense of functionality. With age, MuSCs increased expression of a tumor suppressor, N-myc down-regulated gene 1 (NDRG1), which, by suppressing the mammalian target of rapamycin (mTOR) pathway, increased their long-term survival potential but at the cost of their ability to promptly activate and contribute to muscle regeneration. This delayed muscle regeneration with age may result from a trade-off that favors long-term stem cell survival over immediate regenerative capacity.
How a broken DNA repair tool accelerates aging
Although DNA is tightly packed and protected within the cell nucleus, it is constantly threatened by damage from normal metabolic processes or external stressors such as radiation or chemical substances. To counteract this, cells rely on an elaborate network of repair mechanisms. When these systems fail, DNA damage can accumulate, impair cellular function, and contribute to cancer, aging, and degenerative diseases.
One particularly severe form of DNA damage are the so-called DNA–protein crosslinks (DPCs), in which proteins become attached to DNA. DPCs can arise from alcohol consumption, exposure to substances such as formaldehyde or other aldehydes, or from errors made by enzymes involved in DNA replication and repair. Because DPCs can cause serious errors during cell division by stalling DNA replication, DNA–protein crosslinks pose a serious threat to genome integrity.
The enzyme SPRTN removes DPCs by cleaving the DNA-protein crosslinks. SPRTN malfunctions, for example as a result of mutations, may predispose individuals to developing bone deformities and liver cancer in their teenage years. This rare genetic disorder is known as Ruijs-Aalfs syndrome. Its underlying mechanism remains poorly understood, and there are no specific therapies.
Teaching NeuroImage: Miliary Perivascular Space Enhancement in Sepsis-Associated Posterior Reversible Encephalopathy Syndrome
Plants display a wide range of life spans and aging rates. Although dynamic changes to DNA methylation are a hallmark of aging in mammals, it is unclear whether similar molecular signatures reflect rates of aging and organism life span in plants. In this work, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, which causes DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging can be manipulated by extending or curtailing life span and that shoot apical meristems are protected from these epigenetic changes. We demonstrate that a program of transcriptional repression suppresses DNA methylation maintenance pathways during aging and that mutants of this program display a complete absence of epigenetic decay while physical aging remains unaffected.
DNA-Protein Crosslinks Explain Accelerated Aging in Progeria
In Ruijs-Aalfs progeria syndrome, patients experience accelerated aging and liver cancer.
Now, scientists showed that mutations in a certain gene prevent cells from repairing DNA damage during mitosis, triggering inflammatory immune responses that may fuel premature aging.
Read more.
Researchers have shown that harmful bonds between protein and DNA fuel immune attack in progeria. Pumping up a protein that cuts these bonds could prevent symptoms.
CLN3 mediates chloride efflux from lysosomes
Lysosomes degrade damaged organelles and macromolecules to recycle nutrient components. Lysosomal storage diseases (LSDs) are linked to mutations of genes encoding lysosomal proteins and may lead to age-related disorders, including neurodegenerative diseases. But, how lysosomal dysfunction contributes to neurodegenerative diseases is not clear yet…
The researchers identify CLN3 (ceroid lipofuscinosis, neuronal 3), linked to Batten disease as a conserved lysosomal protein that regulates lysosomal chloride homeostasis, pH, and protein degradation.
Curcumin analog C1 is a natural compound with anti-inflammatory properties could enhance CLN3 activity and improve lysosomal function by activating TFEB. sciencenewshighlights ScienceMission https://sciencemission.com/CLN3-n-chloride-efflux-n-lysosomes
Wang et al. identify CLN3 as a conserved lysosomal protein that regulates lysosomal chloride homeostasis, pH, and protein degradation. Transcription factor EB (TFEB) activation enhances CLN3 function, revealing the TFEB-CLN3 signaling axis as a promising therapeutic target for lysosomal storage disorders.