Lifeboat Foundation: Safeguarding Humanity
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Category: life extension

Inhibiting a master regulator of aging regenerates joint cartilage in mice

An injection that blocks the activity of a protein involved in aging reverses naturally occurring cartilage loss in the knee joints of old mice, a Stanford Medicine-led study has found. The treatment also prevented the development of arthritis after knee injuries mirroring the ACL tears often experienced by athletes or recreational exercisers. An oral version of the treatment is already in clinical trials with the goal of treating age-related muscle weakness.

Samples of human tissue from knee replacement surgeries—which include both the extracellular scaffolding, or matrix, in the joint as well as cartilage-generating chondrocyte cells—also responded to the treatment by making new, functional cartilage.

The study results suggest it may be possible to regenerate cartilage lost to aging or arthritis with an oral drug or local injection, rendering knee and hip replacement unnecessary.

Scientists Reveal Turning Point When Your Body’s Aging Accelerates

The passage of time may be linear, but the course of human aging is not.

Rather than a gradual transition, your life staggers and lurches through the rapid growth of childhood and the plateau of early adulthood, to an acceleration in aging as the decades progress.

A study has identified a turning point at which that acceleration typically takes place: at around age 50.

Your body may already have a molecule that helps fight Alzheimer’s

Spermine, a small but powerful molecule in the body, helps neutralize harmful protein accumulations linked to Alzheimer’s and Parkinson’s. It encourages these misfolded proteins to gather into manageable clumps that cells can more efficiently dispose of through autophagy. Experiments in nematodes show that spermine also enhances longevity and cellular energy production. These insights open the door to targeted therapies powered by polyamines and advanced AI-driven molecular design.

Aging Scrambles Brain Proteins — And Diet Could Partly Reverse It

As we get older, our brains start to change in ways that make them increasingly vulnerable to disease – and a detailed new study of these changes points to a way some of this wear and tear might be prevented or reversed.

Researchers from the Leibniz Institute on Aging – Fritz Lipmann Institute in Germany used mass spectrometry to analyze the balance of brain proteins in both young and old mice, finding differences in a process called ubiquitylation as the animals aged.

Ubiquitylation adds chemical tags to proteins, telling the brain which of these busy molecules are past their peak and should be recycled. In older mouse brains, the ubiquitylation tags really start to pile up on certain proteins.

How a key protein helps drive healthy longevity by maintaining a precise balance

Researchers at Bar-Ilan University have discovered how the longevity-associated protein Sirt6 orchestrates a delicate molecular balancing act that protects the body from age-related decline and disease. The new findings, just published in the Proceedings of the National Academy of Sciences, reveal how Sirt6 preserves health during aging and may pave the way for therapies that promote a longer, healthier life.

Sirt6, often described as a master regulator of aging, is known for its powerful protective effects against age-related diseases such as cancer, diabetes, inflammation, and frailty. Its impact closely resembles that of calorie restriction, a dietary regimen proven in animals to extend lifespan and enhance the body’s natural repair and healing mechanisms.

Calorie restriction—eating fewer calories without malnutrition—has long been known to improve health and extend lifespan. One of its key effects is to increase the body’s production of hydrogen sulfide (H2S), a tiny gas molecule that supports wound healing, heart health, and brain function. This new study found that as we age, H2S levels naturally decline, weakening these protective benefits.

Mitochondrial DNA Acts as a “First Hit” for Antibody-Mediated TRALI

Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related mortality, but its pathogenesis is complex and not well understood. TRALI is thought to develop under a “2-hit” model. In 80% of cases, the second hit is caused by antibodies (specifically anti-HLA class I or II or anti-human neutrophil antigen antibodies); bioactive lipids, extracellular vesicles and other storage-related transfusion products have been linked to the remainder of the TRALI cases. The first-hit, which is related to the patient’s underlying clinical condition, is less well defined. Since patients receiving intensive care are more prone to TRALI and often have elevated levels of extracellular mitochondrial DNA (mtDNA), researchers used a murine model to examine whether mitochondria, mtDNA or other damage-associated molecular patterns (DAMPs) can act as a first-hit in an antibody-dependent murine model of TRALI. Injection of purified mitochondria or mtDNA followed by a monoclonal antibody (as a second-hit) caused significantly greater lung injury with increased pulmonary edema, elevated plasma macrophage inflammatory protein-2 (MIP-2; the mouse ortholog of human IL-8), enhanced neutrophil lung infiltration, hypothermia, and respiratory distress compared to an isotype control. Researchers found that an antagonist to toll-like receptor-9 (TLR-9) attenuated many of the TRALI-like symptoms in mice suggesting that mtDNA and TLR-9 may be involved in the first-hit in some TRALI cases. Targeting mtDNA or the TLR-9 receptor may prove to be a novel therapeutic strategy to prevent the first-hit and TRALI, but further research is needed.

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